Shibly Rahman Paces

Revision Notes for
MRCP 2 PACES
Revision Notes for

MRCP 2 PACES
Shibley Rahman
MA MB BChir PhD (Cantab) MRCP (UK) LLB (Hons)
British Lung Foundation

London (UK)
Avinash Sharma
MBBS MRCP (UK)
Consultant Physician
Luton and Dunstable NHS Foundation Trust
Luton, UK
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Revision Notes for MRCP 2 PACES

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PREFACE
The authors had two principal aims in writing this text: namely,
(i) to explain the ethos and format of the examination, and (ii) to
provide a core body of information useful for the examination. Whilst
this examination is demanding, it is still essentially simply an
assessment of basic competence required for higher specialist training.
The Royal College of Physicians believe that have developed an
examination, which they intend to be fair and to be an appropriate
test of postgraduate knowledge in Doctors preparing for higher
specialist training and since 2001 the examination has been running
very successfully. The academic aims of the MRCP(UK) examination
are stated clearly:
To test a wide range of up-to-date medical knowledge so that
physicians in training are encouraged to develop their full clinical
and professional potential;
To maintain and improve the practice of clinical medicine;
To provide a sound basis for continuing medical education.
Much of this book has been derived from authors; own experiences
regarding the examination, and where possible sample instructions
have been given for individual cases in the real examination. However,
the content of the book closely follows the syllabus as published in
the MRCP Clinical Guidelines. The authors to their knowledge have
been aware of all of these cases having appeared in the Membership
clinical examination at least once.
Management issues/guidance/protocols are all subject to change
with time, and therefore the reader is advised to supplement his/her
reading with other sources, for example, from the Royal College of
Physicians or the National Institute of Clinical Excellence.
Whilst the delivery of the examination is possibly subject to change
with modernisation of the medical curriculum, the content of the higher
specialist training is unlikely to change in the imminent future. Please
consult the www.mrcpuk.org website for current schedules. The
marksheets are available in the Clinical Guidelines and on the website.
Much of this book has been derived from a synthesis of teaching
and examining for the examination nationally in the UK, although the
standards in international centres are exactly the same as in the UK.
vi
The authors wish to emphasise that whilst there is much factual

material in this book, this examination is essentially a test of clinical
skills, and candidates with much general medical clinical experience
pass and those who do not have this experience fail.
As in all good movies, any reference to a real person in the fictitious
scenarios contained in this book is purely coincidental. Good luck!
Shibley Rahman
Avinash Sharma
ACKNOWLEDGEMENTS
Dr Rahman would like to acknowledge his parents and relatives for
their invaluable inspiration. Dr Sharma would also like to thank Laura
for her unending support.
CONTENTS
1. The PACES Carousel ..................................................................... 1
2. Abdominal System (Station 1) ................................................... 8
3. Respiratory System (Station 1) ................................................. 34
4. History Taking (Station 2) ......................................................... 57
5. Cardiovascular System (Station 3) ......................................... 119
6. Central Nervous System (Station 3) ...................................... 154
7. Communication Skills and Ethics (Station 4) ..................... 204
8. Focussed Clinical Problem (Station 5) .................................. 284
Index ............................................................................................... 343
The PACES Carousel
WHY PACES?
PACES is the acronym for Practical Assessment of Clinical Examination
Skills, the practical component of the MRCP examination. It was first
held in June 2001 replacing the previous clinical (long case and short
cases) and oral examination. The introduction of a huge revision of
the examination involved major changes for candidates, examiners,
teachers, local organisers, and central administration throughout the
world.
What are the Aims of the PACES Examination?

The aims of the PACES examination have been clearly stated in the
curriculum (MRCP(UK) Part 2 Clinical Examination (PACES) and clinical
guidelines 2001/2). They are to:
Demonstrate the clinical skills of history taking
Examine a patient appropriately to detect the presence or absence
of physical signs
Interpret physical signs
Make appropriate diagnosis
Develop and discuss emergency, immediate and long-term
management plans
Communicate clinical information to colleagues, patients or their
relative
Discuss ethical issues
How does the PACES Carousel Work?

Five candidates rotate through five 20 minute stations, separated by
upto 5 minutes for change-over and waiting (Fig. 1.1). The cycle begins
with a five minute wait which enables candidates at the two talking
stations (stations 2 and 4) to read the introductory material, whilst

the other three hopefully relax. The whole cycle therefore lasts 125
minutes; it can be entered at any station and, thereafter, the five
candidates follow the same sequence. Two of the clinical examination
stations are double stations; two systems, respiratory and abdominal,
at station 1, and cardiovascular and central nervous, at station 3, are
each examined for ten minutes. Station 5 is now an assessment of a
focussed clinical problem of the type that you might be expected to
see in higher specialist training.
Figure 1.1: Carousel of PACES stations
The talking stations, stations 2 and 4, begin with an al limportant

waiting period outside the room, when the candidates read the
instructions and introductory material and should devise an action
plan for what is to follow. Within the station, they will spend 14
minutes talking to the patient/subject or surrogate, followed by one
minutes reflection, during which the subject usually leaves the room
and, then, a five minute discussion with one or both examiners.
Time
Time-keeping is a key to success for both the PACES examination and
the candidate to succeed. The traditional system of bells and verbal
The PACES Carousel 3

warnings are used together with additional prompts, for a slow
candidate running out of time. Bells are rung at the beginning and
end of the five 20 minute stations and, usually, at 10 minutes in the
two double stations (1 and 3). The examiner will often draw the
candidates attention to a clock, or, better still, will start a stop clock
in the room. In the two talking stations (2 and 4), a verbal 2 minutes
warning will be given at 12 minutes. Time management is also
increasingly important in every clinicians daily work. Although, it is
not explicitly tested in PACES, it is implicit in the strict, but relevant,
time limits set to undertake the various tasks.
It may occur to the candidates that if they prolong their time
examining a patient, it may shorten the discussion time (and, of course,
potential hostile questions). This is not advisable; although examiners
will award some marks for the candidates examination technique
they are observing, the majority of marks will go to the candidates
correct clinical findings, the interpretation of them in a diagnosis or
differential diagnosis, and discussion of further relevant management.
As in all examinations, the way to avoid difficult questions is for the
candidate to be pro-active and try, if possible, to control the discussion
by talking good sense. Most examiners will not interrupt them if what
they are saying is relevant. Examiners get irritated by the slow
candidate who, in addition, may go back to repeat their examination,
suggesting a lack of confidence in their findings.
The times allocated for the tasks you are given at each station, and
substation, are realistic by the standards that apply in everyday
practice. On exception to this, which was soon appreciated by PACES
examiners, is that candidates would not have time to perform a full
neurological examination, in the detail specified in the guidelines, in
the time allocated. The solution lay in the introduction to the case
where candidates should be directed specifically to which part of the
CNS they would be required to examine, e.g. the arms, the legs,
the cranial nerves, speech etc. Such limitation placed on the
examination of a particular system should not preclude the candidate
from saying in their presentation that he or she would investigate
further. A generous examiner would even supply the missing
information!
If you are uncertain about the instructions given relating to the
examination, or any other aspect of the case for that matter, please
ask the examiner for clarification. Examiners will frequently ask the
candidates, after they have read the written instructions, Do you
understand?
Marksheets
You must be familiar with the contents of the seven marksheets as
they are the cornerpiece of the PACES examination. They are easily
accessed, either on the website, or in the Regulations (free), in the
references above. More than recording the marks awarded, they
contain the necessary demographic information and detailed
breakdown and checklist of the component parts of each problem
posed at each station. This is essential to the fairness of the marking
systems and also enables detailed feedback to be given to candidates,
as well as forming the basis of counselling on the rare occasions that
this is recommended.
Each marksheet has four sections and, partly, uses boxes to be
filled using a 2B pencil, to facilitate computer scanning:
1. Candidate
The candidate prints their NAME and fill in their EXAMINATION
NUMBER and the CENTRE NUMBER boxes on each of the seven
pairs of sheets handed to them by the organising registrar (the sheet
number boxes corresponding to the station is already filled in).
2. Examiner
The examiners write in (a box) a brief description of the CASE followed
by PRINTING and SIGNING their name, and, finally, their
EXAMINATION NUMBER.
3. Conduct of Case
Except for Station 5 (Marksheet 7), which is appreviated, there are
three parts for the four major clinical substations.
At stations 1 and 3, the first part is headed Physical examination,
followed by bullet points relevant to that system; the second part is
headed Identification and interpretation of physical signs with three
bullet points: Identifies abnormal physical signs correctly,
Interprets signs correctly, and Makes correct diagnosis. The third
part is headed Discussion related to the case with two bullet points:
Familiar with appropriate investigation and sequence and Famililar
with appropriate further therapy and management.
These second and third parts are identified for the four major
systems (marksheets 1, 2, 4 and 5) and examiners are expected for
each of the three parts to fill ONE of the four boxes: Clear pass, pass,

fail, clear fail. Station 5 (marksheet 7) is divided into the four minor
systems examined and each, in turn, subdivided into the three parts
discussed above (which now become bullet points as there is no room
on the sheet to subdivide them further). For each of the four systems
overall the examiner is required to fill ONE of the four boxes as above.
The crucial part of each marksheet is the bottom line mirroring life.
The box in the bottom right-hand corner requires the examiner to
make an overall judgment using the same four item scale which is
translated into marks: clear fail 1 mark, fail 2 marks, pass 3
marks, clear pass 4 marks. Adjacent to it is a Comments box which
every examiner must complete to explain the decision to give a fail or
clear fail. If the examiner is particularly concerned about some aspect
of the failure which needs to be further explored with the candidate,
another adjacent box, Counselling Recommended, is filled in. This
will NOT automatically lead to the candidate being counselled but
will be discussed with the other nine examiners, at the completion of
the cycle, to decide whether further action is required.
The format of the marksheets for the two talking stations, Station
2 (History Taking) (Marksheet 3) and Station 4 Communication Skills
(Marksheet 6) have the same tripartite structure as those for the major
clinical systems, appropriately adapted, but requiring each examiner
to fill in boxes, as well as, identical to the other sheets, the overall
judgement, comments, and counselling boxes. Thus, the first part of
Marksheet 3, is Data gathering in the interview. The second is
Interpretation and use of information gathered, and the third,
Discussion related to the case, all with appropriate bullet points,
and the examiner (and candidate). Similarly, in marksheet 6, the three
parts are headed Communication skills conduct of interview,
Communication skills exploration and problem negotiation and
Ethics and law (The bullet points are described below under the
two stations).
The marksheets can be downloaded from the official MRCP
website: http://www.mrcpuk.org/Pages/Home.aspx
Marking System
The overall judgement that determines each examiners mark is not
intended to be the numerical mean of the intermediate assessments
made in the various sections of marksheets 1 6, or, even, of the
separate marking of the four minor systems in marksheet 7. This is
because each box filled does not carry equal weight. The value of the
multiple judgements is primarily in providing feedback to candidates

but also enhances broad objective marking by the examiners. It may
help to avoid that they be not overimpressed by one thing the
candidate has done well, ignoring several things not well done, or
vice versa. A further aid to the examiners, available to candidates at
the same sources as the marksheets, are the anchor statements. Thse
try to give substance to the four gradings in assessment, under six
headings: System of examination, Language and communication
skills (in patient encounters when examining clinical systems as well
as the tarking stations, Confidence and rapport, Clinical method,
Discussion and appreciation of patients concerns and Clinical
thinking. When writing comments on a candidate who is being given
an overall fail or clear fail, examiners are encouraged to select
appropriate statements that define the mark; evenn if the patient
achieves an overall pass or clear pass, it can still be helpful to point
out deficiencies (along the way) as an individual examiner will know
nothing of the assessment by the other nine examiners until afterwards.
The pass mark for each of the three diets of PACES held annually
is agreed by the Clinical Examining Board at end of the examination.
The maximum mark attainable by a candidate is to receive a clear
pass from each examiner at every station or substation: 14 4 = 56.
The minimum mark would be 14 1 = 14. An ideal cut off would be
that the candidate should get a pass from each examiner: 14 3 = 42.
Often the pass mark is simply 41.
Examiners
Examiners are widely recruited. There is no lower age limit but they
will usually have been consultant physicians, or equivalent, for atleast
4 years, and have been elected FRCP of one of the UK colleges. They
must have some acute general medicine content in their working
practice; therefore, superspecialists may not be eligible but can
contribute to question-setting. Examiners usually retire within 1 to 2
years after retirement from active clinical practice. Increasing emphasis
is placed on examiner training at regular sessions and briefing before
each examination. Observation of an examination, before actually
examining, is mandatory. Others with an interest in the examination
(teachers, course organisers, examiners from other colleges, and
disciplines) may also observe and their non-participatory role will be
made clear to the candidate.
The performance of examiners is remarkably consistent. Before
each carousel, the paired examiners will see the patients or role players

(surrogates) together and assess the ease or difficulty of a case. They
will agree the criteria they will use in independently awarding the
four grades/marks available. When the candidate has left the
examination room each examiner completes the marksheet and puts
it into a collecting box before finding out the co-examiners mark.
There is exact concurrence within one mark in over 95% of candidateexaminer encounters and exact concurrence in 60%. If necessary, a
brief discussion of any discrepancy within a pair takes place before
the next candidate enters.
Patients
It is a privilege that patients help with the examination, and it is
therefore it is vital that you are as courteous and kind as possible to
the patients. Failure to introduce yourself to and respect these patients
a point which will be repeated in this text is unacceptable. Many
patients are nervous about participating, and also are concerned about
saying something that we fail you. Please be courteous to them. Many
patients ask afterwards how successful you have been and are
genuinely concerned you do well!
Aseptic Techniques
It would be a disaster for the Royal Colleges if patients attended the
examination and then developed some form of transferred infection
such as MRSA which can be tracked back to the examination. Aqueous
gel or hand-washing facilities should be available, and should be used
between all patients.
REFERENCE
MRCP(UK) Part 2 Clinical Examination (PACES): A review of the first four
diets (June 2001 June 2002). J Dacre, GM Besser and P White on behalf of the
MRCP(UK) Clinical Examining Board. J R Coll Edinb 2003;33:285-92.
Abdominal System
(Station 1)
INTRODUCTION TO EXAMINATION TECHNIQUE

There are actually probably only a limited number of causes that are
suitable for the PACES examination!
A good examination technique is critical. Do look carefully and do
feel right up to the costal margins. Many candidates use the light
palpation to look primarily for areas of tenderness, but if you are
careful to use the technique properly it is often possible to feel the
liver and spleen at this stage. If you feel an organ during light palpation,
you can then check the edge more carefully during deep palpation.
You can also check for movement on respiration at this stage.
METHOD OF EXAMINATION TECHNIQUE

Inspection
There are a number of features which are readily found on inspection
(Fig. 2.1). The first thing to note is the nutritional status of the patient.
However, there are many other signs. Look for any surgical scars.
Figure 2.1
Abdominal System (Station 1)
It is important to observe the general appearance of the patient,

which might be suggestive of particular diagnosis, e.g. 1-antitrypsin
deficiency (should be considered if signs of chronic airways disease
are evident on inspection barrel chest, purse lips, respiratory
distress), or Wilsons disease: dystonic movements together with
Kayser-Fleischer rings on slit-lamp. Other common features are
cachexia, icterus, excoriation and bruising. Jaundice is usually detected
clinically when the serum bilirubin level is more than 40 mol/litre.
Tattoos can also be seen, and may be relevant to a liver case.
Look at the shape of the abdomen: The candidate should be able
to recognise different shapes of abdomen and understand their
significance (e.g. symmetry or asymmetry, flatness or distension,
hernias). Previous surgery (e.g. laparoscopy, laporotomy), stretch
marks, intertrigo, haemorrhage, evidence of superficial veins and
direction of flow.
Examine the skin for certain features: colour (anaemia, jaundice,
pallor, ashen grey of Addisons disease), the evidence of previous
surgery (e.g. herniotomy, laparotomy), monilial infection, bruising
and evidence of superficial veins, and evidence of pigmentation
(telengectasia, spider naevi, hyperpigmentation of palmar creases).
Scratch marks would suggest pruritus (cholestasis). Loss of secondary
sexual hair may signify genital hypoplasia. Examine for skin movement:
The candidate should be able to recognise abnormal movement with
respiration, visible peristalsis, or pulsations.
Examine the hands: Confirm the findings on inspection, feeling in
particular for the nodular contracture of Dupuytren or any xanthoma
at the elbow, parotid swelling, fetor hepaticus. Clubbing (chronic liver
disease, inflammatory bowel disease), leukonychia (low protein state),
koilonychias, Beaus lines, Dupuytrens contracture, palmar erythema
(Causes: Cirrhosis, hyperthyroidism, rheumatoid arthritis, pregnancy,
polycythaemia). One can examine for a flapping tremor if one suspects
that the patient is encephalopathic: A coarse flap (need to evaluate
for 30 s to safely rule out presence).
Examine the eyes: Note any xanthelasma around the eyes. Any
arcus (white rim) is often seen around the pupil in those aged 40 and
above. Look for conjunctivae pallor (retract lower eyelid) and scleral
icterus (retract upper eyelid).
Examine the mouth: There are several clinical signs to be found in
the mouth, including angular cheilitis (iron deficiency), glossy red
stomatitis (B12 deficiency or Kawasaki disease), ulcers within the oral
cavity (Crohns disease), telengectasia (hereditary haemorrhagic),
10 Revision Notes for MRCP 2 PACES

pigmentation at the vermilliform border (Peutz-Jehgers), buccal
hyperpigmentation (Addisons disease).
Look for evidence of superficial veins: Look for these determine
the direction of flow (away from umbilicus = portal hypertension;
upwards from the groin = inferior vena cava obstruction). Common
causes of inferior vena cava obstruction are trauma, thrombosis, renal
cell carcinoma, retroperitoneal fibrosis, radiation therapy, aortic
aneurysm, ascites, surgery, filter replacement, and cancer in the vena
cava. Whatever the cause, patients usually develop additional or
collateral veins to compensate for the occlusion. As the flow is towards
the head, not away from the umbilicus (as in caput medusae of portal
hypertension), the two can be delineated.
Examine for lymphadenopathy: Briefly examine from the front
for Virchows node (left supraclavicular fossae). If enlarged nodes
are present, a more comprehensive examination may be required.
Ideally sit the patient up. This will also enable you to look for
nephrectomy scars at the lower back. You can also palpate for inguinal
lymphadenopathy. It is not a good idea to miss lymph nodes if you
are to perform this examination.
Other Considerations
Inspect the antecubital fossae for the presence of arteriovenous
fistula (polycystic kidney disease).
Look for scars in the iliac fossae and lumbar regions (nephrectomy
and transplanted kidney).
Different shapes of abdomen (symmetry/asymmetry, flatness or
distension). Is the entire abdomen enlarged (ascites) or are there
identifiable masses within the abdomen (transplanted kidney). Ask
the patient to lift only his or her shoulders off the bed to reduce
any hernia that may be present.
Dont forget to look at the umbilicus, where a superficial
carcinomatous nodule may be present (Sister Mary Josephs
nodule).
Note any gynaecomastia in the male breast. (Causes: Physiological,
puberty and senility; Klinefelters syndrome; cirrhosis; drugs, e.g.
spironolactone and digoxin; testicular tumour/orchidectomy;
endocrinopathy, e.g. hypo/hyperthyroidism, Addisons disease).
Are there any pulsatile masses? Look for visible peristalsis.
11
Palpation
The mark scheme clearly states that organomegaly or masses should
be correctly palpated. Candidates need to be able to estimate the size
of an organ (e.g. liver, spleen) and to differentiate the organs that are
palpable from each other. As well as kidneys, liver and spleen, other
swellings may be due to:
Gallbladder.
Pelvic masses (e.g. bladder, uterus, ovary). The bladder and bowel
may be felt in normal individuals. The bladder rises out of the
pelvis in the mid-line and pressure may induce a desire to micturate.
Faeces in the bowel can be idented by the examining finger, a
unique feature.
Solid masses (e.g. cancer of the stomach, caecum, abdominal lymph
nodes).
Cystic masses (e.g. pancreatic, mesenteric, ovarian). A pancreatic
pseudocyst, if large, can be felt in the epigastric region; they feel
fixed and do not extend.
Pulsatile swelling (e.g. hepatic, aortic); place both hands on either
side of the mass. Remember that the abdominal aorta bifurcates at
the level of the umbilicus and may be easily palpable in thin patients.
Always test for expansile pulsation which is present with aortic
aneurysm but not if the pulsation is being transmitted. Auscultate
over the swelling, a loud bruit (in the absence of a similar bruit in
the heart) supports the diagnosis of aneurysm. The normal diameter
of the aorta is 3 cm.
Table 2.1: Common causes of abdominal masses
Right iliac fossa
Left iliac fossa
Carcinoma of the caecum

Crohns disease
Appendix mass
Carcinoma of the colon

Diverticular abscess
Less common
Less common
Ileocaecal TB
Ovarian cyst
Pelvic or transplanted kidney
Iliac lymphadenopathy
Crohns disease
Ovarian cyst
Pelvic (or transplanted) kidney
Iliac lymphadenopathy
(Causes of an epigastric mass are discussed later)
Percussion
Percussion to estimate the size of an organ (e.g. liver, spleen).
Percussion should also be used to assess ascites, if considered
appropriate.
Auscultation
The mark scheme includes that the candidate is expected to auscultate
for bowel sounds increased, normal, absent, and bruits arterial,
venous hum. A succussion splash may also be heard.
Conclusion of the Examination

The candidate should close with other relevant features of the
abdominal examination.
One may offer to examine the external genitalia and rectum, but
MRCP Clinical Guidelines state candidates must not perform rectal
or vaginal examinations.
Offer to perform a urinary dipstix, especially in the renal case.
Ask for the temperature chart, BP, urinalysis, oxygen saturations.
The candidate should have acquired the ability to recognise:
Nasogastric tube, gastrostomy, continuous ambulatory peritoneal
dialysis or other dialysis catheter, ileostomy or colostomy,
nephrostomy or vesicostomy, indwelling central venous access device
for parenteral nutrition.
Common Cases
Once the abnormal signs have been elicited, they need to be presented
correctly. The signs should be interpreted correctly within the context
of a diagnosis or differential diagnosis. Common abdominal cases
are listed below, along with related discussion of investigation and
sequence, therapy and management.
CHRONIC LIVER DISEASE

This person who has been abstinent from alcohol for 5 years was
found to have some abnormalities on a GP review for a mortgage.
Please examine his abdomen to see if you can find any abnormality.
Look for Dupuytrens contracture, parotid hypertrophy, features
of Wernickes encephalopathy, features of dilated cardiomyopathy.
Conditions with which Dupuytrens contracture are associated are:
alcoholism, chronic antiepileptic therapy, systemic conditions such
as diabetes, cirrhosis, epilepsy and tuberculosis, thickening of the
corpora cavernosa of the penis (Peyronies disease), Garrods
knuckle pads, and retroperitoneal fibrosis.
Other features (tattoos, track markers).
Leukonychia, clubbing, palmar erythema.
13
Spider naevia (small capillary angiomas found in the distribution

of the superior vena cava in chronic liver disease) and caput
medusae.
Pallor/anaemia.
Paucity of body hair.
Muscle wasting.
Purpura and bruising may be seen in patients with
thrombocytopaenia and coagulation defects.
Small testes.
Ascites and ankle peripheral oedema.
Autoimmune disease (autoimmune hepatitis)
Xanthelasma (primary biliary cirrhosis).
Causes of chronic liver disease: Alcohol, viral hepatitis, autoimmune
chronic active hepatitis, primary biliary cirrhosis, haemochromatosis,
cryptogenic, cardiac failure, constrictive pericarditis, Budd-Chiari
syndrome, biliary cholestasis, toxins and drugs (methotrexate,
methyldopa, isoniazid, amiodarone), Wilsons disease, 1-antitrypsin
deficiency, other metabolic causes.
Causes of palmar erythema: Cirrhosis, hyperthyroidism, rheumatoid
arthritis, pregnancy, polycythaemia.
Causes of cirrhosis: Chronic alcohol abuse (parotid enlargement, multiple
fractures), viral hepatitis (HBV or HCV infection, i/v drugs),
autoimmune disorders (primary biliary cirrhosis, primary sclerosing
cholangitis; ANA and anti-SMA antibodies are positive), genetic
disorders ( 1 -antitrypsin deficiency, Wilsons disease,
haemochromatosis), others (Budd-Chiari syndrome), drugs (e.g.
amiodarone, methyldopa and methotrexate).
Complications of cirrhosis: Variceal haemorrhage, hepatic encephalopathy,
spontaneous bacterial peritonitis.
Investigations of cirrhosis: Liver screen, coagulation screen (PT, APTT,
TT), liver ultrasound, liver biopsy, ANA, dsDNA, anti-smooth muscle
and mitochondrial antibodies, 24 hours urinary copper and serum
caeruloplasmin, serum ferritin, viral hepatitis serology (hepatitis B
and hepatitis C), 1 -antitrypsin levels, immunoglobulins, EEG for
encephalopathy.
Alcohol misuse is characterised by raised -GT, MCV,
thrombocytopaenia, and low urea; although psychiatrists may make
use of urine toxicology and hair samples.

Evidence of decompensation: Altered consciousness, ascites, liver
flap.
Evidence of treatment: Ascitic drain, surgical scars.
Treatment of chronic hepatitis C infection is usually reserved for
those patients with persistently elevated transaminases, increased
hepatitis C viral load and changes on liver biopsy. This treatment is
with peg interferon- and standard dose ribavarin. Assessing a patient
with hepatitis C involves FBC, U&E, LFTs, HCV viral load and
phenotype, -FP, abdominal ultrasound and arrangements for an
elective liver biopsy to exclude fibrosis.
ASCITES
This 55-year-old lady noticed some swelling of her tummy, and she
feels that she has become more itchy because of a longstanding food
allergy. Please examine her abdomen and report your possible
diagnosis.
In the exam, the most frequent cause reflecting epidemiology of
liver disease probably is alcohol, with primary biliary cirrhosis, right
heart failure, and intra-abdominal malignancy less so. Rarely untapped
look for needle marks and comment. Prepare to answer questions
about the management of ascites/sepsis.
Ascites: Abdominal distension, fluid thrill and shifting dullness, everted
umbilicus.
Useful background investigations are: Urinary dipstix (nephrotic
syndrome), FBC (infection), LFTs (deranged in liver disease), and u/
s abdomen (confirms ascites and presence of intraabdominal masses).
The causes can be listed by virtue of the protein content of ascitic
fluid:
Transudate (<25 g/l): Congestive cardiac failure, constrictive
pericarditis (elevated JVP, shortness of breath, third heart sound),
Meigs syndrome (ovarian fibroma, ascites, pleural effusion),
hypoproteinaemic states/nephrotic syndrome (generalized oedema,
proteinuria), cirrhosis.
Exudate (>25 g/l): (Cirrhosis (portal hypertension)), peritonitis,
malignancy (abdominal, pelvic, peritoneal mesothelioma), myxoedema
(hypothyroidism), Budd-Chiari syndrome (hepatic vein obstruction),
portal vein thrombosis, tuberculosis, chylous ascites (obstruction of
lymphatics, e.g. surgery, lymphoma).
15
Other measures include serum ascitesAlbumin gradient measurement;

ascitic leucocyte and neutrophil count or lymphocyte count:
Spontaneous bacterial peritonitis is confirmed when ascitic leucocyte
count > 500 or neutrophil count > 250 cells/high-power film.
Ascitic fluid should be analysed using cell count and differential,
protein, albumin, amylase (pancreatic ascites), glucose (low in bacterial
infections), bilirubin (elevated in bile ascites), cholesterol (raised in
chylous ascites), cytology (malignant ascites), Gram stain. The
macroscopic appearance of ascitic fluid is also important straw
coloured (most causes), turbid (pyogenic causes, TB), bloody
(malignancy, TB), chylous (pancreatitis).
Pathophysiology of ascites: It is assumed that the theoretical aspects of
ascites are examined in the written parts of the examination. However,
candidates should not be made to look embarrassed without a basic
mechanism as it underlies potential treatment pharmacologically (and
these issues may come up in the discussion). Over 75% of ascites is
due to liver disease. The pathogenesis is uncertain, but contributing
factors include hypoalbuminaemia and portal hypertension. It is also
likely that peripheral vasodilatation promotes sodium and water
retention by stimulating the renin-angiotensin-aldosterone system.
There is reduced colloid osmotic pressure and decreased renal blood
flow as a result of splanchnic vasoconstriction.
Portal hypertension is usually the sequelae of cirrhotic liver disease,
whereby the portal pressure in the portal vein is abnormally raised to
more than 10 mmHg. The portal vein enters the liver at the porta
hepatis and sends a branch to each lobe. When portal flow is
obstructed, either from within or outwith the liver, collateral circulation
develops to carry blood to the systemic veins. Extrahepatic obstruction
is caused by increased resistance to flow, e.g. portal or splenic vein
thrombosis. Other causes can include post-hepatic obstruction from
hepatic vein thrombosis (Budd-Chiari syndrome), or extrinsic
compression of the porta hepatis from lymph nodes (prehepatic).
Intrahepatic obstruction is usually due to cirrhosis, right heart failure,
sarcoidosis and schisosomiasis (worldwide). Varices are commonly
oesophageal, derived from the left gastric vein. The clinical
consequences of portal hypertension are gastrointestinal bleeding,
caput medusae, venous hum, splenomegaly (but the size correlates
poorly with portal pressure) and secondary hypersplenism (can cause
peripheral blood cytopaenias). The pressure in the tributary veins is
raised because of back pressure. Features include gastrointestinal

bleeding, caput medusae, venous hum, splenomegaly, and secondary
hypersplenism.
Investigations and management of particular significance to the
acute presentation of alcohol liver disease: Blood tests include blood
cultures and random ethanol level. PT and albumin are important
prognostic factors (Maddreys index- 4.6 increase in PT over normal
+ bilirubin; poor prognosis if >32). Ultrasound of the abdomen
(confirm portal hypertension). Exclude other causes of an acute
hepatitis (hepatitis A IgM, hepatitis B sAg and hepatitis B eAg, liver
autoantibodies, immunoglobulins). Give 5% i/v dextrose if not
hyponatraemic. Treat for alcohol withdrawal before patient develops
signs. Review medications (avoid sedatives). Have a low threshold
for giving broad-spectrum antibiotics once cultures taken.
Management of variceal bleeding: It is useful to be aware of the risk of rebleeding being dependent upon the severity of liver disease, large
varices, varices near the oesophagogastric junction, red sign on
varices, age > 60 years, haemoglobin < 8 g/dl, and renal failure. The
management of variceal bleeding consists of resuscitation,
catherisation, use of vasoconstrictors (e.g. terlipressin, a vasopressin
analogue), balloon tamponade (risk of aspiration), endoscopy with
appropriate therapy (sclerotherapy, ligation with rubber bands and
combination therapy), and TIPPS/surgery (see below). Spontaneous
bacterial peritonitis (SBP) complicates variceal bleeds; the risk is high,
therefore use prophylactic antibiotics when indicated.
Management of ascites: This involves identification and treatment of
any underlying remediable cause of liver disease, e.g. alcohol, strict
sodium and fluid retention, the latter especially if the sodium is very
low, bed rest and diuretic therapy, often requiring combination therapy
of a loop diuretic such as frusemide, together with a potassium sparing
diuretic such as spironolactone. If this fails, bumetanide or metolozone
should be considered. <4060 mmol of salt daily is ideal but difficult
to achieve; <80 is more reasonable. Therapeutic paracentesis may be
necessary for tense ascites, and occasionally concurrent administration
of albumin is indicated. Repeated therapeutic paracentesis should be
avoided as the ascites just reaccumulates and only increases the risk
of peritonitis which can decompensate the underlying liver disease.
Transjugular intrahepatic portosystemic (TIPPS) shunting creates
a side-to-side anastamosis between the portal and hepatic veins in
order to relieve the high venous pressures. It decompresses a high
17
pressure portal system, and is very effective at stopping bleeding in

around 90%. However, it does not influence mortality therefore,
sometimes used in less severe liver disease. Complications include
encephalopathy, infection, bleeding and stent stenosis. Other methods
of shunting in diuretic-resistant ascites are peritonoeovenous shunting
(Le Veen shunt), where a subcutaneous silastic catheter is used to
drain the fluid into the jugular vein, and the Denver shunt (a
modification adding a small subcutaneous pump that can be
compressed externally).
Complications: Spontaneous bacterial peritonitis, pleural effusion,
inguinal, femoral or umbilical hernia, mesenteric venous thrombosis,
functional renal failure.
SPLENOMEGALY
This man has felt discomfort in his tummy. Please examine his
abdomen and discuss your findings with the examiners.
The functions of the spleen are to produce IgM, capture and process
foreign antigen. It filters especially capsulated microorganisms, e.g.
pneumococcus. It sequesters and removes old red blood cells and
platelets. It recycles iron and pools platelets (30% of total platelets
within the spleen).
Usual position of the spleen: 9-11th ribs. A solid organ mass in the left
hypochondrium; candidates often feel too close to the midline or miss
the spleen because they did not feel it on light palpation then missed
the edge on deep palpation. It should be dull to percussion, if it is not
a kidneyatleast identify the inconsistency. Splenomegaly is supported
by the inability to get above or ballot the mass. It usually moves on
respiration. The splenic notch on the superiomedial edge is rarely
palpabledo not forge physical signs. The differential diagnosis of a
LUQ mass includes large left colon cancers, an enlarged spleen, a
pancreatic mass (mainly a carcinoma of the tail), and enlarged left
kidney.
Look for signs of anaemia, lymphadenopathy, and enlarged splenic
edge to beyond the umbilicus.
Signs of infective endocarditis: Splinter haemorrhages, murmur,
etc. Look for rheumatoid hands.
Examine for hepatomegaly.
Enquire about foreign travel and symptoms of possible
haematological malignancy.
Causes of Splenomegaly
Mild
a. Portal hypertension: Did you see signs of chronic liver disease?
b. Lymphoproliferative conditions: Hodgkins lymphoma, chronic
lymphocytic leukaemia or a low grade (follicular) lymphoma are
possibilities because the patients often have stable disease with
organomegaly. If you are allowed to look for nodes, do so, but do
it properly, missing them is not a good idea.
c. Myeloproliferative syndromes: Primary proliferative polycythaemia
(increased red cell mass with normal erythropoietin; predominantly
a disease of middle-aged and elderly, with facial plethora, suffusion
of conjunctivae and engorgement of retinal vessels; presents with
headaches, lethargy, dyspnoea, fluid retention, bleeding, weight
loss, night sweats or pruritus which are exacerbated by a hot bath;
neutrophil alkaline phosphatase (NAP) score is high) or
myelofibrosis, both stable disorders with good signs, chronic
myeloid leukaemiausually treated so that spleen disappears and
therefore uncommon in the examination.
d. Infection (EBV, infective endocarditis, infective hepatitis).
Moderate
a. Lympho-/myeloproliferative disorders
b. Infiltration (Gauchers and amyloidosis).
Massive
a. Myeloproliferative disorders (CML)
b. Myelofibrosis
c. Tropical infections such as visceral leishmaniasis and malaria, rare
in the exam is there a travel history?
d. Hairy cell leukaemia
e. Storage disorders (such as Gauchers disease).
Other Causes
a. Storage disorders: Rare and often treated, so that signs are missing
so uncommon in the exam,
b. Haemoglobinopathies: Sickle rarely gives splenomegaly in adults,
thalassaemia intermedia is possibleusually a mediterranean
person,
19
c. Hereditary spherocytosis is a possible cause (icteric, splenomegaly

and anaemia),
d. Infection EBV,
e. Feltys syndrome (leg ulcers, neutropenia, rheumatoid arthritis).
A quick summary of important haematological malignancies
Chronic myeloid leukaemia is an abnormal proliferation of mature
granulocyte precursors in the bone marrow that arises as a result of
genetic aberration in these cells. WCC is high (50500 109/L) and
thrombocytosis. NAP score is low. This results in the constitutive
activation of tyrosine kinase receptor in those cells that occurs following
juxta-position of the abl gene with the bcr inducer gene. Karyotype
analysis reveals the Philadelphia chromosome in 95% of patients.
Natural history: Initial chronic phase of chronic myelopoiesis
progresses inevitably to an accelerated phase with new cytogenic
changes and finally to blast cell crisis). Anaemia and a high platelet
count often coexist. Splenomegaly may cause pain and abdominal
distension. The condition is treatable with hydroxyurea which lowers
the white cell count and reduces the size of spleen, and is now treatable
with metabolic receptor blocking agent as well as bone marrow
transplantation.
Chronic lymphatic leukaemia is the most common leukaemia and tends
to occur in the elderly, with widespread lymphadenopathy and
moderate hepatosplenomegaly or splenomegaly. Look under armpits. There may be a petechial rash and pallor. There are mutations in
B lymphocyte precursors. CLL is not curable. The long natural history
means that patients may remain asymptomatic and die from an
unrelated problem. Treatment is for symptomatic disease, aiming to
decrease tumour cell load since CLL is not curable.
Polycythaemia rubra vera (PRV) is predominantly a disease of middle
age and elderly. There is often facial plethora, suffusion of the
conjunctivae and engorgement of retinal vessels. It may present with
headaches, lethargy, dyspnoea, fluid retention, bleeding, weight loss,
night sweats or pruritus. Polycythaemias are characterised by an
increased haemoglobin concentration, packed cell volume and RBC
count. Platelet count is also usually elevated. Treatment includes
venesection and hydroxyurea. Causes of secondary polycythaemia
are arterial hypoxaemia, abnormal release of oxygen from haemoglobin
(e.g. carboxyhaemoglobinaemia, interference with tissue oxygen
metabolism), and physiologically inappropriate erythropoietin
production (e.g. neoplasms such as hepatocellular, renal cell cancer

and haemangioblastoma). The diagnosis of PRV has almost been one
of exclusion, but there is increasing interest in the JAK2 mutation as it
affects the phosphorylation of erythropoietin as a possible genetic
test, whilst it is not specific to PRV. One candidate was given an onset
of chorea in a 80-year-old patient, and it turned out that he was told
that the underlying cause in the patients case was PRV!
Hodgkins disease (associated with Reed-Sternberg cells,
lymphadenopathy, splenomegaly, and B symptoms (fever, night
sweats and weight loss) and Non-Hodgkins disease (low-grade
indolent course but can transform to high-grade; high-grade
aggressive disease; bone marrow and CNS are sometimes involved).
Myelofibrosis: Fibrosis in the bone marrow, resulting in extramedullary
haemopoiesis in the liver and spleen.
Investigations: Further examination for nodes, full blood count, film
with markers on blood for diseases such as CLL, CT chest/abdomen/
pelvis for staging of disease, histology, cytogenetics and molecular
genetics for classification of haematologial malignancy and are of
prognostic significance, biopsy of lymph nodes, Coombs test (if
anaemic), ESR, liver ultrasound, ANA, RhF, C3/C4, dsDNA, ACE,
blood cultures, viral serology (hepatitis, HIV), urinalysis haematuria
(endocarditis), proteinuria (myeloma), thick and thin films for Malaria,
echocardiogram, brucella antibodies.
Further Notes
Splenectomy: Causes include rupture (trauma), but splenectomy is
indicated when splenomegaly results in hypersplenism (destruction
of all blood cell types), most often the case in hereditary spherocytosis,
Gauchers disease, autoimmune haemolytic anaemia and thalassaemia.
Other indications include symptoms of mass effect from massive
splenomegaly. Appearances of the blood film post splenectomy are
an increased platelet count and large platelets, increased neutrophils,
and nucleated red cells with Howell-Jolly bodies and target cells.
Patients should be informed pre-operatively of the life-long risk
of simple infections and the need to take prophylactic antibiotic cover
with oral penicillin and the need for immunisation against the common
pneumococcal pathogens (pneumovax). Splenectomy work up is 2/52
prior vaccination against pneumoccocus, meningococcus, Hib,
prophylactic penicillin and medicalert.
Note causes of generalized lymphadenopathy: Lymphoreticular disorder,
chronic lymphatic leukaemia, infectious mononucleosis (likely to be
21
tender), sarcoidosis, tuberculosis, brucellosis, toxoplasmosis,

cytomegalovirus, thyrotoxicosis, progressive generalized
lymphadenopathy of HIV. Investigations include lymph node biopsy,
CT scan and ENT examination.
POLYCYSTIC KIDNEYS/RENAL ENLARGEMENT

This 48-year-old lady, whose only recent medical history includes
headaches, noticed occasional discolouration of her urine, but she
reports that she loves eating beetroot. Please examine her abdomen
and discuss your findings with the examiners, particularly in relation
to what you will advise about next.
An Extremely Common Case

It is important to be able to distinguish between a kidney and a liver:
The liver moves down with inspiration, the kidney being a
retroperitoneal structure moves very little with respiration.
The kidney can be bimanually ballotted, the liver cannot.
The percussion note overlying the liver is usually dull (unless it is
cystically enlarged), whereas it is usually resonant over the kidney
due to superposition of bowel loops.
Examining hand can get between enlarged kidney and costal
margin.
Evidence of renal replacement therapy look for arteriovenous
fistulae at wrist/forearm.
Bi/unilateral ballottable masses in the loin regions with little or
no movement with respiration, and transplanted kidney in the right/
left iliac fossa.
Liver cysts causing irregular hepatomegaly.
Kidney transplant: Look for the characteristic J-shaped scar in the
iliac fossa. Side effects of immunosuppressive treatment.
Anaemia is uncommon due to overproduction of erythropoietin.
Neurological deficit: Associated Berry aneurysms, resulting in
subarachnoid haemorrhage in the minority of patients.
Adult polycystic kidney disease is an autosomal dominant
condition affecting 1 in 400 to 1000. It may cause renal impairment,
hypertension and haematuria.
Cysts in the liver may also occur (more common in infantile
polycystic disease) producing nodular liver enlargement/
hepatomegaly. Cysts may develop in the pancreas, spleen and brain.
There is a predisposition to mitral valve prolapse. Other associations

include berry aneurysms of the cerebral arteries (be attentive for signs
of focal neurological defect). PKD1 is on chromosome 16 and encodes
for polycystin-1, PKD2 is situated on chromosome 4 and codes for
polycystin-2.
Differential diagnosis of a renal mass: Renal cell carcinoma
(associated with weight loss, lymphadenopathy and paraneoplastic
syndromes), hydronephrosis, adrenal massphaeochromocytoma,
carcinoma.
Adults generally present with polycystic kidney disease: Pain,
haematuria, recurrent urinary tract infections, sensation of a mass/
loin pain, polycythaemia, family history.
Complications include loin pain from bleeding into cysts/infected
cysts, mitral valve prolapse, anaemia of chronic renal failure, chronic
renal failure, polycythaemia, distal renal tubular acidosis, cerebral
aneurysms and subarachnoid haemorrhage.
Look for blood pressure, family history and haematuria.
In adults, there is a genetic linkage to chromosome 16 of the PKD
locus, and the condition is inherited in an autosomal dominant manner.
In children, there is linkage to chromosome 4, and the trait is inherited
as an autosomal recessive manner. Children and siblings with
established ADPKD should be offrered screening. Poor prognostic
factors include male, polycystin-1 mutations, early onset hypertension,
episodes of gross haematuria. Incidence 1:1000.
There are bilateral masses in the flanks that are ballotable and the
patient may appear uraemic or may have evidence of an arteriovenous
fistula, permacath or a Tenckoff catheter for dialysis. Polycystic kidneys
are frequently left in-situ following transplantation, so also check for
a mass with an overlying scar in the right iliac fossa.
Uraemic symptoms are anorexia, nausea and vomiting, cramps and
restless legs, peripheral neuropathy, cognitive disturbance and
drowsiness, hiccups, itch, pericarditis symptoms, myoclonus. Three
things to assess in renal failure are uraemic symptoms, fluid status
(fluid overload is indicated by hypertension, elevated JVP and sacral/
peripheral oedema), and metabolic/biochemical status.
Factors which cause a progressive decline in renal function are
hypertension, poor glycaemic control, persistent proteinuria (reduced
with ACEIs and ARBs), dyslipidaemia corrected with statins, smoking,
hyperphosphataemia and anaemia. Smoking needs to stop.
Treatment includes bed-rest and analgesia for pain, treatment of
acidosis if present, nephrectomy/dialysis/renal transplant (patients
require regular renal monitoring as 80% of patients have endstage
23
renal failure by their 8th decade). Hypertension should be carefully

controlled as it may result in deterioration of renal function and
predispose to an intracranial event. Family members should be
counselled and screened with ultrasound cysts can be identified at
about 18 years of age (currently there is no widely available genetic
test), a positive family history of subarachnoid haemorrhage requires
MRI scanning of the brain, as 20% will have a cerebral aneurysm.
Causes of unilateral enlargement:
a. Simple cysts
b. Renal cell carcinoma
c. Polycystic kidney disease
d. Hydronephrosis.
Causes of bilateral enlargement:
a. Polycystic kidney disease
b. Bilateral renal cell carcinoma (5%)
c. Bilateral hydronephrosis
d. Amyloidosis.
Investigations: U & E, urine cytology, ultrasound abdomen + biopsy,
IVU.
- CT if carcinoma is suspected.
- Genetic studies (ADPKD).
RENAL TRANSPLANT
This man feels tired. Please examine his abdomen and discuss your
findings with the examiners, especially in relation to potential
important reasons for his tiredness.

Patients have a scar in the iliac fossa with a smooth ovioid non-mobile
swelling underneath, midline laparotomy scar. Ensure that you look
for signs that the transplant is still functioning an arteriovenous
fistula, permacath, or a Tenckhoff catheter may indicate a return to
dialysis. A good candidate should also pick up on potential causes of
the renal impairment such as adult polycystic kidney disease, diabetes
(lipohypertrophy/lipoatrophy, insulin injection marks, medic alert/
SOS bracelets), SLE or systemic sclerosis. Look also for gum
hypertrophy (ciclosporin), Cushingoid facies, parathyroidectomy scar,
hearing aid (Alports syndrome, Wegeners granulomatosis).

Look for skin signs (malignancy, dysplastic change, SCC, BCC),
Infection (viral warts and cellulitis).
Commonest causes of end-stage renal failure: Diabetes mellitus, hypertensive
renal disease, IgA nephropathy, polycystic kidney disease, bilateral
chronic pyelonephritis.
Aetiology: Lipodystrophy associated with glomerulonephritis,
polycystic kidneys in the abdomen, signs of diabetes, e.g. glucometer,
glucose stix, foot ulcers and poor vision, other autoimmune conditions,
e.g. SLE (rashes), vitiligo.
Differential diagnosis for a mass in the right iliac fossa: Crohns disease,
primary malignancy, iliac TB mass, appendicular abscess, caecal
carcinoid. 2,000 transplants take place in the UK every year, with an
80% 5 years success rate for live donors with one matched haplotype.
Success rates are lower for cadaver kidneys.
Steps taken to ensure graft survival in transplant patients: Preoperatively,
assiduous immunological matching is performed in unrelated donorrecipient pairs including HLA and ABO blood group matching. Blood
transfusions are avoided and any comorbidity minimised, e.g. CABG
performed for chronic angina prior to renal transplant. Live as opposed
to cadaveric donors are preferred, and measures taken to prevent
cold ischaemic damage to allograft.
Postoperatively, immunotherapy is started and continued longterm.
The standard regimen includes: Prednisolone, azathioprine and
ciclosporin, which requires dose monitoring and adjustment. Rejection
is most likely to take place in the first three months. Newer agents
are used to minimize episodes of acute rejection (tacrolimus,
mycophenolate mofetil, monoclonal antibodies directed against the
IL-2 receptor, and sirolimus). Reduction in the dose of ciclosporin (in
patients already taking mycophenolate mofetil and sirolimus) after 1
year may be associated with improved renal function, blood pressure,
lipid and homocysteine levels. There needs to be adequate treatment
of hypertension and dyslipidaemia.
Vascular supply of the transplanted kidney: The donor renal artery is
anastomosed to either the internal or external iliac cartery. The donor
renal vein is reattached to the external iliac vein. The ureter is attached
separately to the patients bladder. The renal pelvis is the most anterior
structure, then artery and vein most posterior.
25
Management of renal transplant patients: Monitor serum creatinine levels,

observe for signs of rejection and secondary malignancy,
immunosuppressive drugs, address cardiovascular risk factors.
Most patients in the exam will have a transplanted kidney that is
functioning well. Symptoms pointing towards graft rejection include
declining renal function, tenderness over the graft, hypertension,
increased shortness of breath (fluid retention) and decreased urine
output.
Types of graft rejection: Hyperacute (preformed antibody mediated ABO
mismatch), acute mixed humoral and cellular response which may
respond to high dose methylprednisolone and/or anti-lymphocyte
antibodies (OKT3), and chronic (cell mediated inflammatory response)
resulting in interstitial fibrosis, and tubular obliteration, is irreversible
and treatment is therefore supportive for the management of chronic
renal failure.
Complications include opportunistic infections (e.g. herpes zoster
virus, Pneumocystis carinii pneumonia, CMV), premature coronary artery
disease, hypertension primarily to ciclosporin, lymphomas and skin
cancers, hypersensitivity reaction and bone marrow suppression
(azathioprine), complications of steroid therapy such as avascular
necrosis of bone.
Increased risk of other pathologies: Seborrhoeic keratosis (increased risk
in azathioprine treatment), skin malignancy, lymphoma, hypertension
and hyperlipidaemia leading to MI and stroke; immunosuppressant
drug side-effects/toxicity: Ciclosporin nephrotoxicity; recurrence of
original disease. Focal segmental glomerulonephritis can recur in
transplanted kidneys. As this results in graft loss in only 15% of
affected patients, it is not a contraindication to transplantation.
Investigations: U&E, FBC (normocytic normochromic anaemia), bone
profile, 24-hour creatinine clearance, renal ultrasound, glucose, HBA1c,
ESR, urinalysis, ANA, dsDNA, ANCA, anti-GBM, C3/C4, RF, serum
protein and urine electrophoresis, antistreptolysin O titre, Hepatitis
B and C serology, prostate specific antigen, renal biopsy.
Features of Therapeutic Intervention

(Renal Replacement Therapy)
Continuous ambulatory peritoneal dialysis (CAPD): 60% of patients
are now treated by this method. The peritoneum acts as a

semipermeable membrane; dialysis takes place via a peritoneal catheter.
Small abdominal scars remain after removal. Uraemic toxins diffuse
into 2-3 litres of dialysate within the peritneum. Excess fluid is removed
by osmosis. Dialysis is required up to three times per day and involves
attaching bags to the peritoneal catheter. Advantages are that it
provides relative freedom from hospital, and is relatively gentle.
The main risk is infection (peritonitis). Contra-indications include
previous abdominal surgery or diverticular disease.
Haemodialysis: This is performed via a fistula in the forearm and the
patients blood is pumped through a dialyser at 200-500 ml/min;
patients often have more than one fistula. Dialysis occurs usually for
3 hours, three times a week in hospital. Satellite dialysis units have
improved patient access. An adequate blood pressure and good
functioning cardiovascular system are required for haemodialysis as
fluid shift is more intense. The advantage is that it is done by others,
but there is a risk of sepsis from access.
CAPD vs. haemodialysis: CAPD is more flexible and can be performed
at home. However, there is a greater risk of infection and the process
needs to be performed three times a day. Haemodialysis requires
more time travelling to a dialysis centre and is less flexible, but gives
superior electrolyte control. Assessment of dialysis patients includes
calculation of their dry weight, looking for potassium and ECG
changes associated with hyperkalaemia, pulmonary oedema and
hypertension.
Complications of dialysis: Acute (peritonitis, bleeding, hypotension, fever,
disequilibrium) and chronic (amyloidosis, malnutrition, neuropathy,
and acquired cystic disease).
There are four life-threatening indications for emergency dialysis
in a known dialysis patient: Serum potassium > 6.5 mmol/l, signs of
fluid overload, worsening acidosis, pericardial rub and other signs of
severe uraemia.
HAEMOCHROMATOSIS
This 46-year-old man who often spends time abroad as part of his job
has asked for advice about skin cancer given his persistent tan. Please
examine the abdomen and discuss with the examiners your thoughts
on his underlying problem.
Inheritance: Autosomal recessive chromosome 6. HFE gene mutation:
regulator of gut iron absorption. Association with HLA-A3.
27
Homozygous prevalence 1:300, carrier rate 1:10. Males affected at an

earlier age due to female protective iron loss by menstruation.
Presentation: Fatigue and arthritis, chronic liver disease, incidental
diagnosis onl family screening.
Signs: (will depend on how late the presentation was and how well
treated). Skin pigmentation, slate grey (associated with deposition of
melanin), sometimes with arthropathy, hepatomegaly, testicular
atrophy, splenomegaly, cardiac disease usually failure. Stigmata of
chronic liver disease such as spider naevi, palmar erythema, ascites,
jaundice. Diabetes mellitus. Arthropathy. Cardiac involvement
(cardiomegaly, congestive cardiac failure). Hepatocellular carcinoma
develops in 33% of cirrhotic patients.
Scars: Venesection weekly until the haemoglobin concentration falls
below 11g/dl and the patient is marginally iron deficient, liver biopsy,
joint replacement, abdominal rooftop incision (this incision is otherwise
known as the double Kocher incision, which allows good access to
the liver and spleen, and is particularly useful for intrahepatic surgery,
radical pancreatic and gastric surgery and bilateral adrenalectomy).
Evidence of advanced liver disease: Loss of body hair, ascites and
gynaecomastia.
Evidence of complications: Endocrine bronze diabetes, congestive
cardiac failure, joints (arthropathy).
Investigations: Fasting serum transferrin saturation > 50% is the best
screening test (remember to suggest checking relatives). Serum ferritin
is markedly raised if there is advanced disease may be normal in
early disease and is not a good screening test. C282Y H63D gene tests
are useful for family studies. It serves as a useful screening tool as
studies have shown that 83-100% of patients exhibit this mutation.
Remember the usual Part 1 catch that ferritin is an acute phase reactant,
and therefore can be raised in an inflammatory process. Liver biopsy
is only required to confirm cirrhosis, usually done if ferritin > 1000
mcg/L.
Management: Aim to have normal transferring saturation and serum
ferritin at around 50. Phlebotomy, most patients tolerate weekly 450
ml maintaining Hb of 12 g/dl. During treatment the serum ferritin
concentration decreases. As iron depletion approaches, serum iron
and Hb concentration falls. The frequency of phlebotomy should be
reduced and a maintenance of 2-6 units removed each year for the

rest of the patients life. Desferroximine as a continuous infusion; a
poor and expensive alternative to phlebotomy. Possibly, avoid alcohol,
Indian Balti curries, and shellfish. Surveillance for HCC.
Family screening: Iron studies. If positive, liver biopsy and genotype
analysis.
Prognosis: 200 X increased risk of HCC if cirrhotic; reduced life
expectancy if cirrhotic; normal life expectancy without cirrhosis and
effective treatment.
Liver transplantation in haemochromatosis: Over 50% 1 year survival, high
mortality: Cardiac + infectious complications.
Consider also blood glucose (diabetes), ECG, CXR and echo
(cardiac failure), liver ultrasound and -fetoprotein (hepatocellular
carcinoma).
CARCINOID SYNDROME
This lady has frequent episodes of diarrhoea. Please examine her
Gut primary with liver metastasis secreting 5 HT into the systemic
circulation.
Symptoms include diarrhoea, wheeze and flushing.
Secreted mediators scar and thicken the right-sided heart valves
resulting in tricuspid regurgitation and/or pulmonary stenosis.
Rarely, a bronchogenic primary tumour can release 5-HT into the
systemic circulation and cause left-sided valve scarring.
HEPATOMEGALY
This 40-year-old man originally from Pakistan has received abnormal
liver function tests, and yet he has never drunk alcohol. He once
received a blood transfusion after a car accident. Please examine his
Start by palpation in the right iliac fossa and move upward with
the fingers of the right hand perpendicular to the costal margin.
Determine the nature of that enlargement (smooth, hard, craggy).
Establish that the mass is truly hepatic by attempting to get above
it.
Establish that the mass, if hepatic, is not just a downwardly
displaced liver (COPD) by percussing downward from the ipsilateral
nipple until dullness is detected.
29
Look for signs of chronic liver disease, lymphadenopathy, no

visually obvious hyperinflated lungs, enlarged liver margin 3-4
breadths below costal margins, smooth and uniformly enlarged or
hard and craggy with irregular edge, gynaecomastia, supraclavicular
nodes, Dupuytrens contracture, raised JVP, jaundice, testicular
atrophy, pedal oedema, absence of secondary sexual hair.
Look for evidence of an underlying cause of hepatomegaly: Tattoos
and needle marks (infectious hepatitis/alcohol), pigmentation
(haemochromatosis), cachexia (malignancy), midline sternotomy scar
(CCF).
If the liver is felt, ascertain the following:
Soft (normal), firm (inflamed or infiltrated) or hard (advanced
cirrhosis or metastases)?
Smooth or nodular if nodular, micronodular or macronodular?
Pulsatile? tricuspid regurgitation (TR)
Tender? TR, Budd-Chiari syndrome, hepatitis, hepatocellular
cancer, abscess
Reidels lobe (a tongue-like projection from the inferior surface of
the right lobe, it can extend to the right iliac fossa).
The differential diagnosis for a RUQ mass includes hepatomegaly,
enlarged gallbladder and colonic carcinoma of hepatic flexure.
Evidence of treatment: Ascitic drain/tap sites and peritonovenous shunts,
surgical scars.
Causes of Hepatomegaly
Physiological (Reidels lobe, hyperexpanded chest)
Infection bacterial (TB, liver abscess), viral hepatitis (EBV, CMV,
hepatitis A, B, and C), protozoal (malaria, histoplasmosis,
amoebiasis, hydatid, schistosomiasis)
Alcoholic liver disease (fatty disease, liver cirrhosis)
Malignant disease (lymphoma, carcinoma or metastatic deposits,
leukaemia, hepatocellular carcinoma, myeloproliferative disorders)
Metabolic/genetic disease (Wilsons disease, AA amyloidosis,
Gauchers disease, haemochromatosis, sarcoidosis, primary biliary
cirrhosis, polycystic disease)
Cardiovascular (right heart failure, hepatic vein thrombosis (expect,
however, ascites and splenomegaly)).
Initial investigations: FBC (for example, raised WCC in infection), ESR,
U&Es, LFTs including albumin and gamma-glutamyl transferase, PT,

APTT, TT, abdominal ultrasound (the first line investigation used to
define the liver architecture, size and clues to the pathology), CXR,
cirrhosis screen, ECG and echocardiography, malignant disease
abdominal CT/MRI scanning (useful to further investigate solid
lesions), -fetoprotein (hepatocellular carcinoma), serum iron and
ferritin levels, serum caeruloplasmin levels and urinary copper levels,
serum blood glucose, Hepatitis viral serology (including hepatitis A,
B, C, EBV, CMV, toxoplasma), autoimmune screen (ANA, dsDNA,
rheumatoid factor, antimitochondrial antibody, antiphospholipid
antibodies), 1-antitrypsin level, serum ACE.
Evidence of decompensation: Ascites, asterixis, altered consciousness.
Differential diagnosis: Enlarged gallbladder, nephromegaly, enlarged
lymph nodes, collection in the Pouch of Rutherford-Morrison, adrenal
tumour, colonic tumour of the hepatic flexure, dilated bowel loops.
It can be difficult to define the edge, if so:
Is percussion helpful?
Does the person look like someone with metastasis?
Are there signs of chronic liver disease, look for hair loss, feel for
gynaecomastia. Prepare to debate what is or is not a spider naevus.
Is there jaundice, tell the examiner that you would like to examine
the testicles in males.
Remember that the patient with cirrhosis may not have a palpable
liver.
Complications of cirrhosis: Variceal haemorrhage due to portal
hypertension, hepatic encephalopathy, spontaneous bacterial
peritonitis.
INFLAMMATORY BOWEL DISEASE

This 27-year-old lady has frequent diarrhoea. Please examine her
Aspects of history: Nature and frequency of blood passed, onset of
symptoms, patients definition of diarrhoea, associated nocturnal
diarrhoea (ulcerative colitis), number of bloody stools per day,
abdominal pain/urgency/tenesmus, straining, constipation and pain
(fissure), rectal lumps/masses, previous GI history (haemorrhoids,
bleeding disorders, food poisoning), drug history (NSAIDs,
anticoagulants, iron and bismuth), alcohol history, FH of GI neoplasia
and polyps, concerns of patient particularly cancer. Systemic features
such as anorexia and malaria.
31
Differential: Colonic cancer, ulcerative colitis, Crohns disease.

Clinical signs: Pallor, anaemia, slim build, oral ulceration, surgical scars,
tenderness, palpable masses (right iliac fossa mass in Crohns disease,
colonic tumour in UC), perianal disease.
Acute severe UC: Usually total disease with severe rectal bleeding and
profuse diarrhoea (> 6 stools/day), abdominal pain, systemic
disturbance (i.e. tachycardia, pyrexia, pallor, wasting). Moderately
active UC: moderate rectal bleeding with some signs of systemic
disturbance, failing to respond to treatment. Mild UC: Little or no
rectal bleeding, no systemic disturbance.
Active Crohns disease: Frank bleeding less common.
Investigation: Stool microscopy and culture to exclude infective cause
of diarrhoea, FBC, inflammatory markers, AXR to exclude toxic
dilatation in UC and small bowel obstruction, sigmoidoscopy and
colonoscopy for histological confirmation, and bowel contrast studies:
Strictures, fistulae in Crohns disease.
Treatment
Medical treatment (including non-pharmacological treatment)
Crohns disease: Smoking cessation. Steroids are the mainstay of
treatment in patients with acute Crohns disease. Tapering steroids
are required to induce remission. A new agent budesonide has a
rapid first-pass metabolism and is poorly absorbed. Maintenance
therapy: Azathioprine, methotrexate, infliximab (particularly useful
for some patients who do not respond to steroids or
immunsuppressive therapy). Metronidazole and ciprofloxacin are
useful as well.
Ulcerative colitis. Oral or topical 5-ASA, i/v steroid and i/v
ciclosporin. Colonoscopic colorectal surveillance is needed and
usually begins no later than 10 yeas after diagnosis.
Maintenance therapy: Oral steroid and 5-ASA.
Nutritional support: High fibre, elemental and low residue diets
Psychological support
Surgical treatment.
Aims of surgery: To restore health in patients with chronic disease, e.g.
nutritional failure. To eliminate the risks of side-effects of steroids in
long-term.

Crohns disease: Obstruction from strictures, complications from fistulae
and perianal disease and failure to respond to medical therapy.
Ulcerative colitis: Chronic symptomatic relief, emergency surgery for
severe refractory colitis and colonic dysplasia following premalignant
change on colonoscopic surveillance or carcinoma.
Emergency surgery is required in perforation, severe
haemorrhage, toxic dilatation > 6 cm (megacolon) as there is a high
risk of perforation and faecal peritonitis, stricture causing obstruction,
fistulae or abscess formation, sepsis.
Complications
Crohns disease: Malabsorption, anaemia, abscess, fistulae, intestinal
obstruction.
Ulcerative colitis: Anaemia, toxic dilatation, perforation, colonic
carcinoma (higher risk in patients with pancolitis 5-10% at 15-20 years),
surveillance (2 yearly colonoscopy for patients with pancolitis > 10
years is usually recommended), colectomy if dysplasia is detected.
Some key extra-intestinal manifestations are shown in Table 2.2.
Table 2.2: Extra-intestinal manifestations
Mouth
Skin
Joint
Eye
Liver
Aphtous ulcers
Erythema nodosum, Pyoderma gangrenosum
Large joint arthritis, Seronegative arthritides
Uveitis, episcleritis, conjunctivitis
Primary sclerosing cholangitis
PRIMARY BILIARY CIRRHOSIS

This 56-year-old lady noticed some changes in the appearance of her
face. Please examine the abdomen to suggest why.
Consider this in a pigmented patient with prominent excoriations
due to marked pruritus and icterus. Look carefully for xanthelasma
and xanthomata over joint, skin folds, and sites of trauma (including
venepuncture). Other xanthomata frequently occur over joints, skin
folds and at sites of trauma. Finger clubbing is common and should
be looked for. The spleen is palpable (50% of cases).
Remember that steatorrhoea in the condition can lead to easy
bruising, osteoporosis and osteomalacia (test for tenderness over the
spine).
Complications: Oesophageal varices, steatorrhoea and malabsorption,
osteomalacia.
33
Important associations: Rheumatoid arthritis, dermatomyositis,

autoimmune thyroiditis, the CREST syndrome, Sjogrens syndrome
and renal tubular acidosis.
Serum antimitochondrial antibody is positive in 95-99%, smooth
muscle antibody positive in 50% and ANF positive in 20%. There is
impaired biliary excretion of copper with excessive copper deposition
in the liver.
Treatment: Ursodeoxycholic acid improves serum biochemistry,
decreases the rate of referral for liver transplantation and decreases
pruritus, but has no effect on histology or long term survival.
HEPATOSPLENOMEGALY
This 50-year-old man has noticed for a long time some lumps in his
neck. Please examine his abdomen and discuss your findings with the
examiners.
No other signs: Myeloproliferative disorders, lymphoproliferative
disorders, cirrhosis of the liver with portal hypertension.
Hepatosplenomegaly with palpable lymph nodes: Chronic lymphatic
leukaemia, lymphoma.
Other causes of hepatosplenomegaly: Malaria (on a world-wide basis),
hepatitis B or C, brucellosis, Weils disease, toxoplasmosis,
cytomegalovirus, pernicious anaemia and other megaloblastic anaemia,
storage disorders, amyloidosis, other signs of portal hypertension
(e.g. Budd-Chiari syndrome).
EPIGASTRIC MASS
The differential diagnosis for this includes gastric carcinoma, pancreatic
pseudocyst, pancreatic carcinoma, and abdominal aortic aneurysm.
Two catches are: (i) Liver (either left lobe or a post-necrotic nodule
of a cirrhotic liver), and (ii) Large recti (these appear to enlarge when
the patient sits forward). You should always suspect gastric or
pancreatic carcinoma in a cachectic patient complaining of pain,
dyspepsia, anorexia and significant weight loss. You may not always
feel a mass.
Characteristics of a gastric carcinoma: Hard, irregular mass, cannot get
above it, and moves with respiration. Think immediately of checking
for a left supraclavicular node (Virchows or Troisiers node).
Characteristics of a pancreatic pseudocyst: Cannot get above it, indistinct
lower border, resonant to percussion, and moves slightly with
respiration.
Respiratory System
(Station 1)

Inspection
The mark scheme makes clear that general inspection is an important
component of the respiratory system examination.
Look for scars: Thoracotomy scar (lobectomy and other thoracic
operations including for treatment of foreign body aspiration,
bronchiectasis, old TB, bronchial carcinoma; note that whereas right
thoracotomy scars are for respiratory procedures left thoracotomy
scars can be used for cardiovascular procedures), aspiration sites for
pleural effusions (often posterior or lateral), and old chest-drains (2nd
intercostals spaces in the mid-clavicular line or 5th intercostals space).
On general inspection, assess the nutritional status (e.g. cachexia).
Look for obvious features of systemic disease, such as:
Pickwickian syndrome: Obese, somnolent, malar facies, audible
wheeze.
Systemic sclerosis: Beaked nose, shiny tight skin over face,
telengectasiae (associated apical fibrosis)
Ankylosing spondylitis: Kyphotic spine (associated apical fibrosis)
Rheumatoid arthritis: Symmetrical destructive arthropathy of the
hands
Horners syndrome: Ptosis, meiosis, enophthalmos, anhydrosis.
Examine for finger clubbing (suppurative lung disease abscess,
bronchiectasis or empyema; fibrosing alveolitis absent in upto 60%,
bronchial carcinoma, mesothelioma) and cyanosis; demonstration of
the flap of carbon dioxide in the hands.
Examine for cyanosis: Are there any additional features of superior
vena caval obstruction (facial and upper limb oedema, dilated
superficial thoracic veins and fixed dilatation of the neck veins), lip
pursing, subcutaneous emphysema?
Respiratory System (Station 1)
35
Assess for respiratory distress: Use of accessory muscles, tachypnoea,

grunting, intercostal/subcostal recession
Listen carefully during your inspection for the sounds of polyphonic
(multiple) or monophonic (large single) wheeze that results from
airways obstruction, particularly in expiration. Is the respiratory cycle
of normal duration (inspiration longer than expiration)? Sounds of
upper airway obstruction may also be evident (grunting, gurgling,
noisy/heavy breathing).
CHEST WALL SHAPES

The Clinical Guidelines report that candidates are expected to be aware
of different types of chest wall shapes. Not only is this important for
the general examination anyway, but the authors are aware of various
instances where this has specifically be enquired about in the actual
MRCP examination (Fig. 3.1).
Kyphoscoliosis: Kyphosis is exaggerated antero-posterior curvature
of the spin. Scoliosis is lateral curvature of the spine. This may be
apparent only as a S shape of the thoracic spine but as the condition
progresses the vertebral bodies are rotated so that the ribs protrude
backwards using a hunch back. This may be idiopathic (80%), or
secondary to polio.
Barrel chest: This is seen in patients with longstanding hyperinflation
of the lungs, as in emphysema and sometimes in kyphosis. This
appearance is due to an increase in AP diameter.
Pectus carinatum: Is protruberant sternum. It may be congenital or
secondary to severe childhood asthma, rickets or congenital heart
disease. It consists of a localised prominence of the sternum and
adjacent costal cartilages, often accompanied by indrawing of the
ribs to form symmetrical grooves (Harrisons sulci).
Pectus excavatum: Is a depressed sternum. This is congenital and
not secondary to lung disease. It may be a forme fruste of Marfans
syndrome and is associated with mitral valve prolapse. The distance
between the spine and sternum is reduced resulting in an apparent
enlargement of the heart on chest radiograph and functional systolic
murmur. The lower end of the sternum is depressed, though when
severe the whole sternum and costal cartilages are sunken. It may
cause a displaced apex beat, cardiac murmur, apparent
cardiomegaly and abnormal lung function if very severe.
Harrisons sulci: These are horizontal grooves at the bottom of the
rib cage in children caused by persistent indrawing of the ribs.

Thoracoplasty: Note any scars from previous surgery or trauma.
Before chemotherapy for tuberculosis was available, a thoracoplasty
consisting of pushing in part of the ribcage to collapse the
underlying lung was sometimes performed.
Chest wall shapes:
Figure 3.1: Chest wall shapes
Purse-lip breathing: Seen in chronic obstructive airways obstruction

(especially emphysema). Not necessarily a sign of distress, as is a
means of increasing the intra-thoracic pressure to collapsed bronchioles.
Rate of respiration: Use of accessory muscles of respiration; symmetry
of expansion (asymmetrical chest wall movement is suggestive of a
reduction in lung volume collapse, pneumothorax, fibrosis or
reduction surgery).
Evidence of previous surgery (e.g. thoracotomy, thoracoplasty,
thorascopic biopsy, plombage) or radiotherapy (e.g. telengectasia,
burns, limb lymphoedema, Indian ink marks for field identification),
37
evidence of engorged superficial veins (e.g. SVC obstruction) or

subcutaneous nodules
Look for a Horners syndrome and wasting of small muscles of
the hand wasting.
Look for signs relating to the skin: the candidate should be able to
recognise associated disease (e.g. eczema), the evidence of previous
surgery (e.g. thoracotomy, chest drain, Portacath), and engorged
superficial veins (e.g. SVC obstruction), subcutaneous emphysema.
Superior vena cava obstruction is most often due to bronchial carcinoma
and/or associated mediastinal glands, lymphoma, and mediastinal
fibrosis and other rare causes. The resulting signs may vary in severity:
dilated veins on the anterior chest wall, engorged fixed non-pulsatile
jugular veins, swollen face, neck and sometimes arms, and conjunctival
oedema.
Surface anatomy: The right lung is divided into three lobes (upper,
middle and lower) while the left lung is divided into two lobes while
the lingula divides the two (Fig. 3.2).
Figure 3.2: Surface anatomy of lungs
Palpation
Examine the hands: Feel pulse (bounding) and examine for the presence
of a flapping tremor (carbon dioxide retention). Confirm correct
position of the trachea with appropriate warning; check for tracheal
deviation by placing the index and ring fingers of the trachea at the
sternal angle and using the middle finger to feel the tracheal rings.
Demonstrate appropriate techniques for assessing the position of
the upper and lower mediastinum. If you attempt to do this from

both sides of the chest, be prepared to give a sensible justification
(e.g. confirmation of findings). Assess both the extent and symmetry
of movement of two sides of chest wall. Ask the patient Could you
please take a deep breath in?. The thumbs should separate by atleast 5
cm. Confirm the findings from inspection by placing a hand either
side of the sternum, and observe any loss of chest wall expansion
during inspiration. Ensure that you have assessed the expansion of
both the upper and lower lobes bilaterally (this requires this
manoeuvre being performed twice; above and below the breast).
Confirm the position of the apex beat, as displacement will signify
mediastinal shift. The impulse may be difficult to feel in the hyperinflated chest.
Assess tactile vocal fremitus or vocal resonance. It is adequate to
do one or the other (some examiners are thought to prefer only vocal
resonance). It may be more fluent to assess vocal resonance, as this
can be done at the end of auscultation. Use the ulnar border of the
hand for tactile vocal fremitus. This is increased over consolidated
lung and diminished when air, fluid or thickened pleural separates
the lung from the chest wall, or when a major bronchus is occluded.
Ask the patient to repeat 99. Is there any aegophany?
Palpate for cervical and axillary lymphadenopathy. Examine the
patients neck from the back and axillae from the front for the presence
of enlarged lymph nodes. If present, determine the character (hard
as in carcinoma, rubbery as in lymphoma or tender as is often the
case as in viral infection).
Percussion
Start in the supraclavicular fossae, comparing the sides then move
down to below the clavicles. In order to adequately assess the
percussion note, you do not have to percuss over every rib space. It is
only necessary to percuss over the area of the underlying lobes. This
means that the same information can be got by percussing in three
places as thirty (remember to percuss in the axillary region to assess
the middle lobe).
Auscultation
Both sides of the chest need to be auscultated for bronchial (lobar
pneumonia) and vesicular breath sounds, the intensity of breath
sounds. Localised decreased breath sounds are found in a
pneumothorax, pleural effusion, tumour, pleural thickening and
collapse. Generalised decreased breath sounds occur in emphysema,
39
asthma, muscular chest wall, obesity and fibrotic lung disease.

Bronchial breathing is heard in consolidation, abscess near a chest
wall, bronchial neoplasm, dense fibrosis and the top of a pleural
effusion. It can also be heard if one is listening too close to the midline.
The chest especially should be examined for added sounds (e.g.
crackles, wheeze inspiratory crepitations/crackles should be timed
for when they occur in the respiratory cycle, as this may be a pointer
to underlying pathology early to mid : bronchiectasis, mid to late
lung fibrosis (fine) or pulmonary oedema; wheeze = the air passing
through an airway that is narrowed and on the point of closure); click
and noises from the chest wall in synchrony with cardiac systole.
Dont forget the lung apices. Is expiration longer than inspiration
(asthma)?
Examine for whispering pectoriloquy or vocal resonance (when
appropriate): Voice sounds conducted through consolidated lung
tissue, extensive fibrosis and pulmonary collapse associated with a
patent bronchus resemble more closely those produced at the larynx
than those heard over normal lungs, in that they are louder and more
distinct.
The presence of a pleural rub (crunching sound during inspiration)
signifies pleural inflammation (usually infection/uraemia).
OTHER POINTS OF THE RESPIRATORY EXAMINATION

The candidate should close with other relevant features of the
respiratory examination, viz:
Sputum pot: Significance of copious mucopurulent secretions
suggesting bronchiectasis.
Presence of oxygen cylinder or nebuliser.
Oxygen saturation monitor: Offer to ask for the oxygen saturation.
Peak flow: Measurement of peak flow measurement using an
appropriate meter.
Bedside spirometry
Arterial blood gas measurement
Tracheostomy: An inference for why the tracheostomy scar is
present.
Inhaler technique: The technique of standard inhaler devices and
their appropriate application.
Inhaler Technique
This has been known to be assessed in PACES within Station 1, Station
2 or Station 4.

Explain the way in which the bronchodilator works: By relaxing the air
passages in your lungs.
Explain the need for the bronchodilator solution: To reach as deep down
into your lungs as possible and to stay in your lungs long enough
to be absorbed.
Remove the mouthpiece cover.
Shake the cannister.
Hold the inhaler vertically in your dominant hand. Dexterity is
important.
Breathe right out.
Put the mouthpiece in your mouth with your lips tightly around it.
Press firmly down on the body of the inhaler as you start to breath
in. This timing is important.
Take in a deep breath slowly so that the spray goes deeply into
your lungs.
Hold the breath for 10 sec.
Breathe out and go through the whole process again.
Common Respiratory Cases

of a diagnosis or differential diagnoses. Common respiratory cases
LUNG MALIGNANCY
This 42-year-old man has been short of breath. Please examine his
respiratory system and discuss with the examiners.
Commonest Malignancy in the Western World

Key Signs
Systemic features: Cachexia, anaemia, clubbing, tar-stained fingers,
tracheal deviation towards collapse or away (effusion) from the lesion,
reduced expansion, percussion note dull (collapse/consolidation) or
stony dull (effusion), auscultation (crackles and bronchial breathing)
and reduced breath sounds and vocal resonance (effusion), HPOA,
lymphadenopathy.
Chest: None, consolidation, collapse, pleural effusion.
Metastasis: Bone tenderness, hepatomegaly.
41
Paraneoplastic: Gynaecomastia, Lambert-Eaton syndrome, SLCL,

squamous cell carcinoma, dermatomyositis and acanthosis nigricans.
Endocrine: Ectopic ACTH production (Cushings syndrome), PTHrp
production (squamous cell carcinoma), SIADH.
Dermatological/rheumatological: Dermatomyositis, clubbing,
hypertrophic pulmonary osteoparthropathy.
Neurological: Confusion, fits, focal CNS deficits, cerebellar
syndrome, proximal myopathy, peripheral neuropathy.
Other features: Superior vena cava obstruction due to mediastinal
lymph nodes compressing the superior vena cava impeding venous
return (suffused and oedematous face and upper limbs, dilated
superficial chest veins and stridor, non-pulsatile elevation of the jugular
venous pressure) (Causes: Bronchial carcinoma, enlargement of the
thyroid or thymus glands, TB, recurrent laryngeal nerve palsy).
Symptoms include painless swelling of the face, headache, visual
disturbance with the sensation of fullness in the ears. Investigations
for SVCO obstruction are chest X-ray, thoracic CT scan, a venogram.
To confirm carcinoma, carry out investigations below. Therapeutic
modalities are radiotherapy or chemotherapy, and corticosteroids are
useful in reducing laryngeal and/or cerebral oedema.
Aetiology: This is predominantly:
1. Cigarette smoking (this causes the vast majority of adenocarcinoma
of the lung),
2. Manufacturing Asbestosis, chromate, nickel, arsenic, radioactivity
uranium mining.
Investigations
These include:
Cytology: Sputum and pleural fluid,
CXR: Opacities, hilar enlargement, consolidation, lung collapse,
pleural effusion, bony secondaries,
FNAC,
Bronchoscopy + washings/brushings/transbronchial biopsy, (if the
tumour is located centrally),
Open/VATS biopsy,
CT, lung function tests,
Radionuclide scans for bony metastasis,
PET of the lung (for certain cases).
The purpose of the investigations is to allow the following:
1. Diagnosis of the mass (CXR: collapse, mass, hilar lymphadenopathy) and spiral CT (so small tumours are not lost between
slices during a breath).

2. Determine cell type (induced sputum cytology, biopsy by
bronchoscopy or percutaneous needle).
3. Stage (CT/bronchoscopy/mediastinoscopy/thoracoscopy). Nonsmall cell carcinoma: TNM staging to assess operability. Small cell
carcinoma: Limited or extensive disease.
4. Lung function tests for operability assessment. Pneumonectomy
contraindicated if FEV1 < 1.2L.
5. Complications of the tumour. Metastasis: Increased LFTs, increased
calcium, anaemia. NSCLC: PTHrP hypercalcaemia, and SCLC:
increased ACTH, SIADH to hyponatraemia.
Treatment
An important aspect, of course, is for the patient to stop smoking if
he/she is still smoking.
In the UK, NICE recommends professional guidance on the
management of lung cancer: This guidance was published in 2005 in
the form of the leaflet CG24, available on their website http://
www.nice.org.uk/nicemedia/pdf/CG024niceguideline.pdf
Surgery for fit patients with early disease (IA, IB, II), involving
lobectomy or pneumonectomy, excision of peripheral tumours,
contraindications to surgery in non-small cell lung cancer: Metastatic
carcinoma, transfer factor < 50%, severe pulmonary hypertension,
uncontrolled cardiac arrhythmias, poor lung function, left laryngeal
nerve palsy, malignant effusion, dysphagia, mediastinal lymph node
involvement, superior vena cava obstruction, phrenic nerve palsy, rib
or distant metastasis.
Curative radical radiotherapy for those who are unfit for surgery
or patients with mediastinal node involvement, neoadjuvant
chemotherapy for small cell tumours before radiotherapy, palliative
radiotherapy for bronchial obstruction, SVC obstruction, haemoptysis,
bone pain, cerebral metastasis, radiotherapy/stenting for SVC
obstruction, endobronchial therapy, pleural drainage/pleurodesis,
drug therapy (symptomatic)
Small cell lung cancer: Chemotherapy benefit with six courses.
Palliative care: Dexamethasone and radiotherapy for brain metastasis
and SVCO, radiotherapy for haemoptysis, bone pain and cough,
chemical pleurodesis for effusion, opiates for cough and pain.
According to the aforementioned NICE guideline, If a chest X-ray
or chest computed tomography (CT) scan suggests lung cancer
(including pleural effusion and slowly resolving consolidation), patients
43
should be offered an urgent referral to a member of the lung cancer

multidisciplinary team (MDT), usually a chest physician.
Finally, an important aspect of advice is access to charities and
support groups, such as those offered by the British Lung Foundation,
the Roy Castle Foundation, and Macmillan Cancer Support.
CHRONIC OBSTRUCTIVE AIRWAYS DISEASE


Causes: Environmental (smoking and industrial dust exposure) and
genetic (-antitrypsin deficiency).
Key signs: Nebulizers/inhalers/nasal speculums/sputum pot and its
contents, signs of hyperinflation, barrel-shaped chest, tracheal tug,
nicotine-stained fingers, low position of the laryngeal prominence,
loss of cardiac dullness, and lowering of hepatic dullness, bounding
pulse, face and conjunctivae for plethora. Tachypnoea, use of accessory
muscles, loss of normal outward movement of the abdomen during
inspiration and expiratory wheeze. Advanced stage: Pursed lip breathing,
cyanosis on the underside of the tongue and vermilion border of the
lip, and in-drawing of the lateral rib cage (Hoovers sign) on
inspiration. Advancing respiratory failure, cyanosis, restlessness,
confusion, coarse tremor and warm peripheries. Percussion note
resonant.
Note COPD does not cause clubbing: Therefore, if present, consider
bronchial carcinoma or bronchiectasis.
Look carefully for evidence of hyperinflation of the chest:
Symmetrical diminution of chest expansion
Increased A-P diameter of the chest (but this may also occur in
disorders of the thoracic spine)
Use of accessory muscles of respiration, especially sternomastoids
Indrawing of intercostals spaces, supraclavicular fossae and costal
margins on inspiration
Shortening of the distance between the cricoid cartilage and
suprasternal notch to less than three finger breadths
Loss of cardiac and hepatic dullness
Hyper resonance of the chest to percussion

Blue bloater: Bronchitis (minimal inflation, dyspnoea, cor pulmonale,
i.e. raised JVP, ankle oedema, RV heave and loud P2, coarse
crepitations): Pink puffer emphysema (hyperinflated barrel shaped
chest, tachypnoea, purse-lip breathing, no pulmonary hypertension/
cor pulmonale). Chronic bronchitis is a clinical diagnosis: Cough
productive of sputum on most days for >3/12 on >2 consecutive years.
Emphysema: Pathological diagnosis: Destruction of alveolar walls.
Degree of overlap with chronic asthma (main differential diagnosis),
although in COPD there tends to be reversibility (<15%).
Cor pulmonale: Cyanosis, respiratory distress, systolic waves in JVP,
malar flush, ankle and sacral oedema, parasternal heave, loud P2 with
a pansystolic murmur heard best in inspiration at the sternal edge.
Cor pulmonale is the enlargement of the right ventricle that occurs as
a consequence to raised pulmonary artery pressure (pulmonary
hypertension) that occurs secondary to chronic lung disorders (e.g.
COAD, bronchiectasis) or disorders of the pulmonary circulation
(recurrent pulmonary emboli, pulmonary hypertension). ECG features:
P pulmonale, right axis deviation, right ventricular hypertrophy.
Investigations: FBCraised WCC (infection), low albumin (severity);
CXRhyperinflation, flat hemidiaphragms, large central pulmonary
arteries, reduced peripheral lung markings, bullae, ABGtype II
respiratory failure, ECGright atrial and ventricular hypertrophy (cor
pulmonale), respiratory function testslow transfer factor and
obstructive (obstructive + air trapping).
Management
[Please note that, in the UK, NICE offers authoritative guideline for
the management of COPD (please refer to the link http://
www.nice.org.uk/guidance/CG12) and the British Thoracic Society
offers guideline for pulmonary rehabilitation (http://www.britthoracic.org.uk/ClinicalInformation/PulmonaryRehabilitation/tabid/
108/Default.aspx).]
Aspects of Management
Weight reduction, if overweight/obese (support for nutritionists
may be sensible here);
Stop smoking through willpower, literature, advice, clinics (such
as stop smoking programmes), psychological intervention, antismoking medication; exercise;
45
Pulmonary rehabilitation empowering patients to take interest and

control of their condition [Please note that the current NICE
guideline recommends that all patients with COPD who are unable
to go about their day-to-day business should be offered a course
of pulmonary rehabilitation classes (The BTS guidelines emphasize
that anyone with chronic dyspnoea whose lifestyle is affected
should have pulmonary rehabilitation this applies mainly to
patients with COPD, but not exclusively)].
Bronchodilators such as 2 receptor agonists (salbutamol) or
anticholinergic inhalers such as ipatropium bromide should be
offered in patients who are breathless. A trial of oral theophylline
should be considered. A trial of corticosteroids may be instituted
using oral prednisolone 30 mg daily for 2 weeks, if there is failure
to respond to increased bronchodilator therapy. Lung function is
measured before and after and an improvement of >15% in airflow
limitation indicates the need for inhaled steroids. If no
improvement occurs then inhaled steroid is unlikely to be beneficial
[The airway defect is largely fixed but may be partially reversible
with the use of bronchodilators. A positive test is one in which
there is > 200 ml increase in FEV 1 from baseline response to
bronchodilator or steroid (a more brisk response of > 500 mls may
indicate asthma rather than COPD)].
Antibiotics when symptomatic of infection. This is particularly
useful (and steroid tablets) for early intervention in an acute
exacerbation of COPD [Also see later; please note that reducing
the amount of re-hospitalizations for patients with COPD is a key
target in the UK National Service Framework for COPD].
Treatment of heart failure, if present.
Surgery is indicated in selected patients only (pleurodesis
procedures for recurrent pneumothraces, bullectomy for isolated
bullous disease and lung volume reduction surgery in emphysema).
Annual influenza vaccination (if no contra-indication).
Long term oxygen therapy: If PO2 < 7.3 and FEV1 < 1.5 litres, evidence
of cor pulmonale. 2-4L via nasal prongs for atleast 15 hrs a day is
effective. Improves average survival by 9 months. The patient must
not smoke and use long-term oxygen therapy because of the
obvious risk of flammability.
Non-invasive ventilation: This is now being used more and more
frequently as a means of avoiding endotracheal assisted ventilation,
from which it is often very difficult to wean patients with COAD
off. It provides pressure support through a face mask and has

been shown to be of benefit in those with hypercapnic hypoxia. It
is sometimes not well tolerated as the mask needs to be tightly
applied to the face. Consider BIPAP when pH < 7.35, hypercapnia,
and respiratory rare > 30. C/I to NIPPV include imminent arrest,
bulbar palsy, coma, and upper airway obstruction.
[Please note that NICE does not recommend 1-antitrypsin
replacement in patients with proven deficiency and severe symptoms].
Acute Exacerbation
Usual precipitants of an exacerbation smoking (triggering
bronchospasm), infection (most commonly H. influenzae, S. pneumoniae
or M. catarrhalis), bronchoconstricting drugs, exercise. Treatment of
an acute exacerbation: Controlled oxygen via Venturi mask 24%,
nebulised bronchodilators, antibiotics, steroids 7-14 days, i/v
aminophylline. Even if the CXR shows no radiological evidence of
pneumonia, antibiotics such as Ofloxacin can still be used in patients
with severe exacerbations (Lancet 2001;358:2913), where the primary
end-point was death in hospital or need for repeat courses of
antibiotics. Follow-up involves assessing the patients ability to cope,
measuring FEV 1 , checking inhaler technique and the patients
understanding of disease and treatment, and assessment of home
nebulizers and LTOT if severe COPD.
Guidelines for specialist referral: Rapid decline in FEV1, COPD in
patients less than 40 years and in patients with less than 10 pack years
smoking, bullous lung disease, severe COPD, assessment for LTOT/
trial of steroids/home nebulizers, frequent infections (exclude
bronchiectasis), symptoms out of proportion to lung deficit, uncertain
diagnosis.
Consolidation
This patient has been acutely unwell for 3 days, with shortness of
breath and a productive cough. Please examine his chest.
Community-acquired pneumonia. Common organisms: Strep. Pneumoniae
50%, Mycoplasma pneumoniae 6%, Haemophilus influenzae, Chlamydia
pneumoniae.
Antibiotics: 1st line: penicillin or cephalosporin and macrolide.
Hospital-acquired pneumonia. Common organisms above plus Pseudomonas,
Staph. aureus, Gram-negative bacilli. Antibiotics: 1st line: Anti-pseudomonal
penicillin or broad-spectrum Cephalosporin + gentamicin.
47
Causes of consolidation: Pneumonia, tumour, pulmonary embolus,

vasculitis, e.g. Churg-Strauss.
Clinical signs: Tachypnoea (count respiratory rate), oxygen mark,
sputum pot (rusty sputum indicates pneumococcus), reduced
expansion and increased tactile focal fremitus, dull percussion note,
focal coarse crackles, increased vocal resonance and bronchial
breathing, ask for the temperature chart. Extra points include:
Confusion and hypotension and markers of severity, complications,
e.g. parapneumonic effusion, clubbing may indicate an abscess,
erythema multiforme (target lesions due to Mycoplasma).
Severity score for pneumonia: CURB 65 (urea > 7; respiratory rate > 30;
BP systolic < 90 mmHg or diastolic <60 mmHg), WCC <4 or >12, T >
38 or <32, age > 65, PaO2 <8 kPa, multiple lobes affected.
Prevention: Pneumovax II to high-risk groups, e.g. chronic disease
(especially nephrotic and asplenic atients) and the elderly.
Investigation: CXR consolidation (air bronchogram), abscess and
effusion; bloods (WCC, CRP, urea, atypical serology, immunoglobulins), blood (25% positive) and sputum cultures, urine (Legionella
antigen, Pneumococcal antigen, haemoglobulinuria: Mycoplasma
causes cold agglutinins causing haemodialysis).
Management: Oxygen and antibiotics.
Complications: Lung abscess (Staph. aureus, Klebsiella, anaerobes), parapneumonic effusion/empyema, pneumothorax, haemoptysis, septic
shock and multi-organ failure.
PULMONARY FIBROSIS/CRYPTOGENIC
FIBROSING ALVEOLITIS

Key signs: Chest wall movement reduced on side of lesion, tracheal
displacement towards side of lesion, percussion note is dull,
widespread inspiratory crepitations, tactile vocal fremitus increased,
clubbing, rheumatoid hands (bibasal fine crackles end-inspiratory if
cryptogenic fibrosing alveolitis). No sputum.

Signs of associated autoimmune diseases: E.g. rheumatoid arthritis (hands),
SLE and systemic sclerosis (face and hands) and Crohns (mouth
ulcers). Signs of treatment: E.g. Cushingoid from steroids. 65-85% of
patients with fibrosing alveolitis have clubbing.
Underlying diagnoses: Connective tissue diseases, SLE, rheumatoid
disease, radiotherapy, drugs, e.g. methotrexate, amiodarone,
sulphalasize, gold, sulphonamides, nitrofurantoin, inorganic dust
related interstitial lung disease, e.g. asbestosis, granulomatous disease
(e.g. sarcoidosis, tuberculosis, beryllosis), offending agents known
to cause hypersensitivity pneumonitis (e.g. mushrooms).
Causes of basal fibrosis: Cryptogenic fibrosing alveolitis, asbestosis,
amiodarone, connective tissue diseases, aspiration.
Causes of upper lobe fibrosis: Pneumoconioses (excluding asbestosis), EAA,
TB, ABPA, ankylosing spondylitis.
Idiopathic cryptogenic fibrosing alveolitis: A histopathological spectrum
from inflammatory dequasamative interstitial pneumonitis to fibrosis
usual interstitial pneumonitis (UIP). UIP is more common. Overall
prognosis is poor, though DIP responds better to steroids.
Desquamative interstitial pneumonitis (DIP) is inflammatory in nature,
whereas UIP is more advanced inflammation with fibrosis. The overall
prognosis in cryptogenic fibrosing alveolitis is poor. The importance
of tests supporting an inflammatory picture is that there is likely to
be a beter response to steroids and immunosuppression.
Complications: 60% of patients die as a direct consequence of fibrosing
alveolitis, pulmonary hypertension and right heart failure, lung cancer.
Investigations: Bloods (ESR, rheumatoid factor, ANA), drug history,
spirometry, autoantibodies, CXR (bilateral basal reticulonodular
changes), ABG for type I respiratory failure, HRCT (groundglass
opacification), bronchoalveolar lavage (lymphocytes predominate in
inflammatory and neutrophils do not), pulmonary function tests
including diffusion capacity, tests for underlying causes. DTPA scan
can be used to assess the probability of deterioration. Serum precipitins
for EAA.
HRCT may obviate need for the biopsy. Open lung biopsy
(transbronchial or percutaneous biopsy may be required for histology).
Management: Depends on the underlying cause. High dose steroids
should be commenced following diagnosis (often involving a highresolution, thin slice CT of thorax) and then continued for 4 to 6 weeks.
If this does not achieve remission, then immunosuppressant drugs
49
such as azathioprine or cyclophosphamide should be considered. Lung

transplantation is an option in younger patients with rapidly
progressive disease: there is a 60% 1 year survival rate.
Prognosis: 50% mortality at 2 years. There is an increased risk of
bronchogenic carcinoma.
Other Points to Note

Apical fibrosis: Possible ipsilateral tracheal deviation, reduced upper
zone expansion, dull percussion note, fine inspiratory crepitations in
upper zone. Causes: Old tuberculosis, radiotherapy, ankylosing
spondylitis, connective tissue disorders (anti-Jo-1 dermatomyositis),
extrinsic allergic alveolitis, massive pulmonary fibrosis from
pneumoconiosis, histoplasmosis.
Other features of old TB: Chest deformity, tracheal deviation towards
the side of the lesion (fibrosis), reduced expansion, dull percussion,
crackles and bronchial breathing, scars from previous plombage
therapy (pingpong balls/sponges used to collapse the infected lobe
to prevent aeration and spread of bacilli), previous lobectomy/
pneumonectomy scars (look at back and under axillae), and scars from
phrenic nerve crush for diaphragm analysis, kyphosis (Potts fracture).
Streptomycin was introduced in the 1950s. It was the first drug shown
to be beneficial in a randomized controlled trial.
Primary TB: Asymptomatic, persistent cough, significant CMI,
compression of a bronchus leading to collapse. TB may progress or
re-activate: Postprimary TB causes endobronchial symptoms (cough,
sputum, haemoptysis), compression of a bronchus by lymph nodes
leading to collapse of a lobe or segment, spread via the lymphatics to
the pleura, aspergilloma formation within a cavitated lesion. Tests:
Tuberculin and Mantoux (strongly positive may imply active infection),
and Heaf. False ves, when CMI response is impaired. CXR (patchy
upper lobe opacification) and microbiological identification (AFB, early
morning urines).
Postprimary TB: This involves necrosis in the centre of the lesion, with
discharge of its contents and cavitation. Discharge into the bronchus
with endobronchial symptoms can occur, compression of a bronchus
by lymph nodes leading to collapse of a segment, spread via the
lymphatics to the pleura or pericardium, and aspergilloma formation
within a cavitated lesions.

Asbestos-related lung disease: Usually occurs > 20 years after exposure,
proportional to the intensity of exposure. Characterized by exertional
dyspnoea, dry cough, inspiratory crackles in lower zones. Chest Xray may show irregular opacities, and with more advanced disease
honeycombing. Pulmonary function tests reveal restrictive lung disease
with a reduced transfer factor. Lung cancer is increased synergistically
with smoking, and the risk of mesothelioma is markedly increased.
Patients are eligible for industrial injury benefit. Benign pleural disease
involves plaques, diffuse pleural thickening, effusion and calcification.
Benign pleural disease is usually asymptomatic and detected on CXR.
Patients are usually not eligible for industrial injury benefit.
Mesothelioma normally occurs > 30 years, and almost always caused
by asbestosis. High risk asbestosis is crocidolite (blue asbestos).
Diagnosis is confirmed by pleural biopsy.
Pneumoconioses: Silicosisupper zone fibrosis with eggshell hilar
calcification that predisposes to TB infection; berylliosis
granulomatous lesions resulting in fibrosis, similar to sarcoid;
asbestosispredominantly affects lung bases, pleural plaques and
associated mesothelioma; simple coal-workers lung does not cause
pulmonary fibrosis.
Extrinsic allergic alveolitis: Bird fanciers lung (pigeons), Farmers lung
(mouldy hay), Byssinosiscotton dust. Following exposure there is
inflammation of the bronchioles resulting in cough, pyrexia and
malaise. If exposure becomes chronic it may result in increasing
shortness of breath and non-caseating granulomatous disease.
Treatment is with steroids in acute disease and long-term avoidance
of precipitating factors.
BRONCHIECTASIS
This 60 or 21-year-old woman presents to your clinic with a chronic
cough. Please examine her chest and discuss your finding.

Bronchiectasis is a term used to describe abnormal and permanently
dilated airways.
Points in the examination: Clubbing, central cyanosis, dyspnoeic and
tachypnoeic, cachexia and short stature, cough with copious purulent
sputum (often bloody) and halitosis, coarse inspiratory crepitations,
often cover one or more areas of lung. Look for cystic fibrosis (CF),
51
post infective (pneumonia, TB, measles, whooping cough), ABPA,

hypogammaglobulinaemia, primary ciliary dyskinesia/Kartageners
syndrome.
CF: Examine the precordium, Portex reservoir under the skin or
Hickman line/scars for long-term antibiotics. CF features: Respiratory,
intestinal (obstruction, rectal prolapse, pancreatic failure and
malabsorption/failure to thrive, diabetes develops in 20% of adults
due to destruction of the islets of Langerhans by mucoid plugging of
the pancreatic ducts, biliary cirrhosis, gallstones, meconium ileus),
infertility, arthropathy.
Cor-pulmonale: Cyanosis, ankle oedema, RVH, loud P2.
Part of the differential of clubbing and crackles includes interstitial
lung fibrosis and malignancy.
Potential complications include anaemia, brain abscess, empyema,
cor pulmonae and secondary amyloidosis, chest pain, haemoptysis,
metastatic spread of infection, arthropathy.
Investigation: Sputum culture and sensitivity and cytology, CXR shows
tramline shadows and high resolution CT scan (thickened bronchial
walls), sinus radiography (mucosal thickening and fluid levels),
aspergillus precipitins. Look for a specific cause: Bronchoscopy for
malignancy, serum immunoglobulins for hypogammaglobulinaemia,
aspergillus precipitins and skin prick testing, and saccharine ciliary
motility tests (nares to taste buds in 30 min): Kartageners syndrome.
CF investigations: Screened at birth by low immunoreactive trypsin.
Sweat test Na+ >60 mol/l (false positive in hypothyroidism and
Addisons disease). Genetic screening.
CF genetics: Incidence 1/2500 live births, autosomal recessive
chromosome 7q, CFTR, commonest mutation is a deletion Df508.
Pathophysiology: Secretions are thickened and the lumens of various
structures are blocked (bronchioles leading to bronchiectasis;
pancreatic ducts leading to chronic pancreatitis, gut leading to
meconium ileus equivalent in adults; seminal vesicles leading to male
infertility).
General principles of treatment: Postural drainage, physiotherapy,
antibiotic therapy for exacerbations particularly to cover Pseudomonas,
mucolytics (nebulised rhDNase is effective in patients with viscid
sputum), longer-term rotating antibiotics, bronchodilators, if there is
any airflow obstruction, surgery is occasionally used for localised

disease, gene therapy for cystic fibrosis, replacement of
immunoglobulins. Specific treatment of CF; daily chest percussion and
physiotherapy, early institution of broad spectrum antibiotics for
minimisation of lung damage from infective exacerbations, pancreatic
enzyme replacement therapy (e.g. pancrease), immunization,
bronchodilators, aerosol dornase alpha which interferes with sputum
neutrophil DNA, immunisation, heart-lung transplantation for poor
pulmonary function and purulent bronchiectasis, palliative care, gene
therapy.
Causes
1. Congenital: Cystic fibrosis Kartageners syndrome (features are
dextrocardia, bronchiectasis, situs inversus, infertility, dysplasia
of the frontal sinuses, sinusitis, otitis media; patients have ciliary
motility).
2. Mechanical: Bronchial carcinoma (suspect if localized bronchiectasis).
3. Childhood infections: Whooping cough, measles and TB.
4. Immune overactivity: Allergic bronchopulmonary aspergillosis.
5. Immune underactivity: Hypogammaglobulinaemia.
6. Aspiration: Chronic alcoholics.
7. Yellow nail syndrome: The nails are thick, excessively curved from
side to side and slow growing, leaving bulbous fingertips
uncovered and pale yellow. The cuticles are lost, the lunulae are
absent and there is oncholysis. The yellow nail syndrome is usually
associated with lymphatic hypoplasia, ankle oedema and a number
of pulmonary conditions such as bronchiectasis, pleural effusion,
COPD and malignant neoplasms. Other associations include Dpenicillamine therapy, nephrotic syndrome, hypothyroidism and
AIDS.
Complications: Cor pulmonale, secondary amyloidosis, massive
haemoptysis, metastatic infection, e.g. cerebral abscess.
ASTHMA
Look initially for pectus carinatum (see chest wall shapes above).
Examination reveals a bilateral scattered wheeze, and costal recession.
Examine the sputum cup, and comment on accessory muscles of
respiration, tachycardia, pulsus paradoxus and whether the patient
can utter sentences without stopping to take a breath. The diagnosis
is bronchial asthma and comment on the functional status.
53
Asthma is an inflammatory disorder characterized by hyperresponsiveness of the airway to various stimuli, resulting in
widespread narrowing of the airway.
Indications for steroids in chronic asthma: Sleep is disturbed by
the wheeze, morning tightness persists until midday, symptoms and
peak expiratory flows progressively deteriorate each day, maximum
treatment is with bronchodilators, emergency nebulizers are needed.
Investigations: Dynamic spirometry, serial peak flow measurement, skin
tests to assess the role of allergens, steroid response test, airways
hyperrespnsiveness test (increased sensitivity to histamine ot
metacholine bronchial provocation test). For acute episodes, peak flow
measurement, arterial blood gases, chest X-ray (to exclude pneumothora
or pneumonia), ECG if the cause of breathlessness unclear, and sputum
culture.
Complications: Retarded growth rate, pneumothorax, thoracic cage
abnormality, recurrent bronchial infection, respiratory arrest, fixed
airway obstruction.
Non-pharmacological management of chronic asthma: Avoidance
of cold air, diet (high intake of fresh fruit and vegetables), clean
mattresses (avoidance of bed mites), removal of other exacerbating
factors (e.g. family pets).
Pharmacological management of a patient with acute asthma:
Nebulised -agonists, e.g. salbutamol, oxygen, high-dose steroids
(intravenous hydrocortisone or oral prednisolone), blood gases, CXR
to rule out pneumothorax.
Table 3.1: Asthma guidelines
BTS guidelines (please refer to the BTS website for the current guidelines)
Step 1
Step 2
Step 3
Step 4
Step 5
Inhaled short-acting -agonists used as required for symptom relief.

Step 1 + regular inhaled anti-inflammatory agents (such as beclomethasone,
budesonide, chromoglycate)
Step 1 + high-dose inhaled steroids or low dose inhaled steroids plus a longacting beta-agonist bronchodilator
Step 1 + high-dose inhaled steroids and regular bronchodilators (long-acting
inhaled or oral beta-agonists, sustained-release theophylline, inhaled ipatropium)
Step 4 + oral steroids
LUNG COLLAPSE
This man is stable, but has had a previous procedure. What was that
procedure, and why might he have done this? Confine your
examination to the respiratory system.

Ipsilateral tracheal deviation, decreased ipsilateral expansion, dull
ipsilateral percussion note, reduced ipsilateral breath sounds.
Common causes of lung collapse: Iatrogenic for TB, bronchial carcinoma,
bronchial adenoma, lymphadenopathy, mucus plugs (asthma, allergic
bronchopulmonary aspergillosis), foreign bodies. Tell the examiner
that you would like to look for tar staining (tobacco smoking), clubbing
and cachexia.
A Note on Pneumothorax
Unlikely to be in the examination, but the author has experience of
some candidates feeling they were given a small apical pneumothorax.
The classification of a pneumothorax is given in Table 3.2.
Contralateral tracheal deviation, reduced ipsilateral expansion,
hyper-resonant ipsilateral percussion note, reduced/absent ipsilateral
breath sounds.
Causes of pneumothorax: Spontaneous (usually in thin males), trauma,
bronchial asthma, COPD, carcinoma of the lung, cystic fibrosis, TB.
Table 3.2: BTS grading of pneumothorax (see BTS guidelines for current guidelines)
Small
Moderate
Complete
Tension
Small rim of air around the lung (those less than 20% in size usually resolve
within weeks)
Lung is collapsed towards the heart border
Airless lung, separate from the diaphragm (aspiration which is less painful
than intercostals drainage, leads to a shorter admission time and reduces the
need for pleurectomy with no increase in recurrence rate at 1 year)
Any pneumothorax with cardiorespiratory distress (rare and requires
immediate drainage)
PLEURAL EFFUSION

Key signs: Tachypnoea, fullness of intercostal spaces, diminished chest
movements on inspection and palpation, apical impulse not visualised,
trachea shifted to the opposite side, vocal fremitus and vocal resonance
reduced on affected size, stony dullness on percussion, diminished
breath sounds. Bleating aegophany may be heard above the level of
the effusion.
Extra points: Cancer (clubbing and lymphadenopathy), mastectomy,
colostomy or laporomy, radiation scars and tattoos, chemotherapy
55
alopecia, mucositis, Cushings syndrome, radiation scars, tuberculosis/

lymphoma (lymphadenopathy and fever), congestive cardiac failure
(raised JVP, third heart sound, peripheral oedema), nephrotic
syndrome (generalised oedema and ascites), chronic liver disease/
cirrhosis (leuconychia, spider naevi and gynaecomastia), autoimmune
disease (characteristic rash or arthritis), pulmonary emboli (raised
JVP, right ventricular heave, loud P2, deep vein thrombosis),
hypothyroidism (dry skin, bradycardia, characteristic facies, slowrelaxing reflexes), chronic renal failure (arteriovenous fistula),
connective tissue disease (rheumatoid hands), signs of DVT.
Differential diagnosis: Consolidation (bronchial breath sounds), collapse,
raised hemidiaphragm, pleural thickening. Dyspnoea on immersion
in water is suggestive of diaphragmatic palsy and therefore perhaps
the most useful diagnostic investigation are dynamic diaphragm
studies.
Causes: Exudate (>30 g/dl protein): Bronchial cancer, pneumonia,
mesothelioma, drugs (methotrexate, nitrofurantoin), TB, rheumatoid
disease, SLE, sarcoidosis, Dresslers syndrome, PE, pulmonary
infarction, metastasis.
Transudate (<30 g/dl protein): Nephrotic syndrome, cirrhosis, cardiac
failure, hypothyroidism, yellow-nail syndrome, peritoneal dialysis,
Meigs syndrome.
Investigations
Blood tests (FBC, ESR, U&Es, LFTs, full biochemical profile,).
CXR (AP and lateral: earliest sign is blunting of the costophrenic
angle which may require the presence of at least 300 ml of fluid).
Aspiration of the pleural fluid (confirm diagnosis, appearance of
fluid? chylous suggests malignancy or trauma to the thoracic duct
and? bloody suggests malignancy, infarction or trauma, type of
fluid exudates or transudate; exudates favoured by protein
concentration pleural fluid: Serum > 0.5, LDH pleural fluid: Serum
> 0.6, highly cellular fluid), smear (Gram stain, Ziehl-Nielsen,
malignant cells), further tests on aspirate (e.g. amylase > 200 units/
dl is indicative of pancreatitis or occasionally malignancy).
Sputum examination (AFB, pneumonia, malignant cells).
Serological tests (RA factor, ANF).
Pleural biopsy (essential for TB and malignancy).
Mantoux test.

Ultrasound of abdomen for hepatic cause.
Bronchoscopy + CT-guided biopsy for tissue diagnosis (biopsy is
useful for diagnosis of tuberculosis and malignancy)/thoracoscopy.
CT or MRI chest depending on underlying cause (looking
particularly for localized effusions and pleural and parenchymal
disease) possibly a bone scan.
Investigations: Pleural fluid cytology (60%) plus pleural biopsy (70%)
plus thoracoscopy (90+%), CT of thorax may also be useful.
Complications: Constrictive fibrosis of pleural and restricted lung
function, iatrogenic secondary infection, iatrogenic pneumothorax,
unilateral pulmonary oedema, and haemorrhage (especially after
pleural biopsy).
Management: The principal aim is to treat the aetiology, aspiration if
causing respiratory distress, pleurodeses, surgery (persistent
collections and for progressive pleural thickening). For infective causes,
systemic antibiotics are indicated and intercostal drainage is essential.
For tuberculosis, standard oral antituberculosis chemotherapy is
indicated. For malignant effusions, pleural effusion indicates
inoperability; treatment is guided by symptoms. Agents (tetracycline,
talc or bleomycin) are introduced via intercostals drains to cause
adhesion of the two layers of pleura and prevent re-accumulation
(pleurodesis).
A Note on Empyema
Empyema is a collection of pus within the pleural space. Most frequent
organisms are anaerobes, staphylococci and Gram-negative organisms.
Associated with bronchial obstruction, e.g. carcinoma. Treatment:
Pleural drainage and IV antibiotics. Intrapleural streptokinase. Surgery.
History Taking
(Station 2)
INTRODUCTION TO THE GENERAL APPROACH TO THE

HISTORYTAKING STATION
[The MRCP Clinical Examining Board have kindly made available
sample scenarios for this Station: these may be viewed and
downloaded using the following link: http://www.mrcpuk.org/
PACES/Pages/PACESscenarios.aspx]
The timing of the station starts when you enter the station having
read the letter. Make sure you take note of the detail in it, and the
particular questions that need to be answered. You will probably be
asked how you will respond to the GPs request for advice, so focus
your history on addressing the problems of relevance, as well as
leaving time for more general enquiry. When starting the conversation
with the patient remember to take time to introduce yourself, put the
patient at ease, and check that the patients understanding of why
he/she is there corresponds to yours as you would in real life. If the
information given by your patient differs from that in the GP letter,
try not to panic. As you know, this happens in real life, and you
should simply clarify the position with the patient, as you would
normally.
Be alert to clues that the patient may give regarding particular
concerns, or emotional state part of the test is to see how good you
are picking these up. Is the patient concerned about cancer; are there
distressing social circumstances behind the presenting complaint?
Towards the end of your time, remember to summarise with the patient
the salient points of the history (this allows you to fill in any detail
that may have escaped you earlier), to share with the patient your
thoughts about the possible nature of the problems, and to explain
briefly how you will take matters forward. This also helps you to
formulate your problem list. The patient is at liberty to ask for an
explanation of any tests you suggest.

1. The key points in the first part of the markscheme, data gathering
in the interview, are:
Presenting complaints are elicited, and documented in a logical
and systematic way.
Inclusion of systems review.
Enquiry about past medical history/family/smoking/treatment
history (past and present). Candidates surprisingly often omit a
drug allergy history.
Do not forget the social history and follow psychosocial clues.
Follows leads about relevant psycho-social factors (including:
Activities of daily living, work life, home life, tobacco, alcohol,
recreational drugs, sexual history, impact of problems on the job).
Appropriate verbal and non-verbal (eye contact, posture etc.)
responsiveness, good balance of open and closed questions.
2 The second part of the markscheme deals with identification and
use of the information gathered. This involves:
Checking information is correct with patient. This is in terminology
appropriate to the patient.
An ability to interpret history with the patient. You should offer
a diagnosis, and then regarding the management go onto
explaining the process, risks and benefits of various options, and
perhaps explaining some uncertainties regarding diagnosis,
outcome or prognosis if relevant. Check for understanding and
summarising at appropriate intervals.
A good candidate would also give the patient the opportunity to
ask any further questions before closure.
An ability to create a problem list including diagnosis, social
problems, concerns or complaints about treatment, and disease
complications, is inherent.
3 The third part of the markscheme deals with discussion related
to the case. In the semi-structured oral interview, the candidate
is expected to:
Be able to discuss the implications of the patients problems, both
medical and referral to surgery and other specialists including
alternative/complementary medicine.
Be able to discuss strategy for solving the problem. This is
terminology appropriate to senior examiners!
In discussing with the examiners, you will be expected to consider
how the patients problems affect lifestyle, social interactions and
employment prospects, as well as the purely medical aspects. You
will probably be asked for a reasonable differential diagnosis on the
History Taking (Station 2)
59
basis of what you have accrued, possibly be asked what signs you
might look for on clinical examination, and be asked for your strategy
for solving the problems so again this may be a series of tests or
may be much broader, and involve other health professionals. Finally,
if there have been any specific questions asked by the referral letter,
you must address them. The examiners will mark your performance
on your handling of the conversation and also the accuracy of
information that you have given. Whilst the emphasis will be on history
taking and communication skills, if you give a patient or relative
seriously misleading or dangerous information you willl be failed.
You will also be failed if you do not ask the key questions that would
materially affect the treatment of the patient, e.g. other medications.
COMMON SYMPTOMS COMPRISING THE HISTORY

Each history and scenario will be different, but the principles above
can still apply. We have included here some common complaints,
both in real life and in examinations both at undergraduate and
postgraduate level. These are broadly divided into subject group,
although some symptoms may cross more than one group.
CARDIOVASCULAR SYSTEM
Hypertensive
Points in the history Has the hypertension been found before? Relevant
symptoms such as cardiac failure, headaches, palpitations, dyspnoea,
ankle oedema, blurred vision, tremors, weight change, renal disease,
anxiety disorder.
Elicit cardiac risk factors (e.g. ethnic origin, cholesterol, smoking,
a relevant family history including relevant disorders renal disease
and neurofibromatosis) and previous medical history (previous MI/
CVA, renal infarction, renovascular disease, diabetes); obtain a drug
history including previous drug history and side-effects (steroids,
NSAIDs, OCP, MAOIs), and some details of lifestyle issues (e.g.
smoking, caffeine and alcohol history, domestic situation and its
accompanying stresses).
Enquire specifically about certain features suggestive of a cause:
For example, weakness in patients with hyperaldosteronism may
suggest hypokalaemia; paroxysmal symptoms, palpitations, sweating,
pallor flushing suggest phaeochromocytoma; features to suggest
Cushings disease (e.g. weight gain, muscle weakness, hair growth)
or acromegaly (headaches, galactorrhoea); pulsation in the neck may
be suggestive of an adult-type coarctation of the aorta.
Causes
The causes of hypertension are generally a white-coat effect, primary
(essential) or secondary. Important secondary causes include intrinsic
renal disease (polyarteritis nodosa, systemic sclerosis, chromic
pyelonephritis, polycystic kidneys, renal artery stenosis either due to
fibromuscular dysplasia or artheromatous disease, Cushings
syndrome, Conns syndrome, acromegaly, hyperparathyroidism,
coarctation of the aorta, pregnancy and pre-eclampsia, steroid therapy.
Investigations
U&Es, cholesterol, glucose, ECG, urine analysis (for protein, blood),
renal ultrasound of the kidneys (e.g. polcystic kidneys, renal artery
stenosis), renal arteriogram, 24-hr urinary VMA, 24-hr urinary free
cortisol, urinary free cortisol, renin, aldosterone, OGTT (acromegaly),
echocardiogram, 24-hour ambulatory blood pressure monitoring for
white coat or borderline hypertension.
Management
This includes measurement of the blood pressure (two subsequent
clinics are needed where their blood pressure is assessed from two
readings using the best conditions available; routine use of automated
blood pressure monitoring or home-monitoring devices in primary
care is not currently recommended because their value has not been
adequately monitored); lifestyle changes initially and then
periodically, drug treatment to patients with persistently high blood
pressure and monitoring of side-effects. Anti-hypertensive drug
treatment initiated in systolic BP > 160 or sustained diastolic > 100
mmHg (<140/90 diabetics). Consider other drugs for cardiovascular
risk, e.g. aspirin, statin therapy. A sustained drop in BP is needed,
and modifiable risk factors should be addressed before
pharmacological treatment is instituted.
Chest Pain
Points in the History
An accurate history of the chest pain is vital: This includes where
(ischaemic pain is poorly localised retrosternal discomfort often
described as tightness, pressure or burning), nature (ischaemic pain
is heavy or tight, often patients deny the symptom of pain and refer
to it as discomfort), radiation (may radiate to the arms, neck, jaw,
61
gums or abdomen, and sometimes this may be the only sites),

exacerbating factors (including exertion effects, posture, meals), cardiac
risk factors. Cardiac pain tends to be heaviness, band, gripping and
dull ache. Precipitants are exertion, cold weather, or stress. Noncardiac pain tends to be a dull ache, sharp, shooting, and precipitated
by specific body motion. Enquire about rest and nocturnal pain. A
history of hot and shivery symptoms, central chest pain comfortable
when sitting upright, inability to sleep lying down, no effect of
exertion and eating is suggestive of pericarditis? may be on the
background of autoimmune disease. Pericarditis is pleuritic chest pain,
varying with posture, classically relieved by sitting forward. Consider
predisposing factors to angina: Including obesity, hyperlipidaemia,
hypertension, hyperthyroidism, anaemia.
Enquire about previous medical history: Cardiovascular or
cerebrovascular disease, cholesterol, diabetes, hypertension, risk
factors for PE/DVT, pericarditis risk factors (pyogenic, TB, malignant,
uraemia, hypothyroid, autoimmune disorders). Include a drug history,
family history of peripheral vascular disease, thrombophilia, familial
hypercholesterolaemia, and social history (smoking, occupational
lifestyle, recent travel).
Differential Diagnosis
(1) Chronic stable angina, predictable on exercise and may be relieved
by rest; worse in cold or windy weather, induced by stress, rapidly
improved by GTN, (2) Unstable angina, at rest, (3) Pericarditis:
Localized anterior central pain, worse on breathing and lying flat, (4)
Aortic dissection, sudden onset radiating to the back, (5) Pleural pain,
lateralized and worse on breathing and associated with cough, (6)
Oesophageal pain (may be worse on eating and associated with
vomiting; oesophagitis may be pain after meals particularly citrus juices
or spirits, with relief on sitting or standing up), (7) Spinal pain, mainly
in the back but may radiate round to front in a nerve root distribution,
(8) Skin pain, usually due to shingles, (9) Musculoskeletal pain, usually
tender to palpation, (10) Pulmonary embolism which may cause sudden
chest pain, hypotension, dyspnoea, collapse and right heart strain.
Investigations
FBC (neutrophil leukocytosis and thrombocytosis in MI), ECG (resting
rhythm, evidence of previous MI, LVH, right-heart strain), glucose,
lipids, CK/troponin I, exercuse testing, CXR (focal lung disease,

masses, pruning of pulmonary vessels as in pulmonary hypertension),
Hb/TFTs (thyroid function can exacerbate pain as can anaemia), V/Q
scan (if PE suspected), echocardiogram (structural heart disease), H.
pylori if suspicion of oesophageal pain (also consider upper GI
endoscopy and oesophageal manometry).
Cardiac Failure
Try to confirm that symptoms are consistent with heart failure in the
first place, for example traditionally with LVF: Dyspnoea, orthopnoea,
paroxysmal nocturnal dyspnoea, nocturnal cough, fatigue. Symptoms
are usually worse when lying flat, but this is not specific: For example,
consider GORD, postnasal drip and bronchial secretions. RVF: Ankle
swelling. Assess symptom severity: The NHYA scale is Ino
limitations, II slight limitation of physical activity, IIImarked
limitation of physical activity; IV symptoms at rest.
Consider the patients thoughts about the causes of the symptoms
and expectations of treatment. What can your patient no longer do
that he/she would like to do? Does he/she live alone? What family,
friends and other supports are there?
Enquire about the possible causes of heart failure: Coronary artery
disease, pressure overload (hypertension or aortic stenosis), volume
overload (aortic or mitral regurgitation), arrhythmias (including atrial
fibrillation), and cor pulmonale (often due to COPD but sometimes
parenchymal lung disease or pulmonary emboli).
Investigations
Ask about investigations so far: Assessment of renal function and
albumin should be included since fluid overload leading to pulmonary
oedema can be due to renal failure or hypoalbuminaemia.
Management
ACE inhibitors improve outcome, and should be used in all patients,
apart from where contraindicated. -blockers have been shown to
improve outcome in selected patients with NYHA I-III classes.
Everyday experience shows that loop and thiazide diuretics improve
symptoms but do not improve outcome. Low dose spironolactone is
useful for NYHA III and IV in those already being treated with ACEI
and diuretics. Digoxin should be considered for all patients with heart
failure and atrial fibrillation.
63
A NEW MURMUR/ENDOCARDITIS
Murmurs are often asymptomatic and discovered during routine
medical examination. New murmurs associated with fever or signs of
infection are indicative of endocarditis. Check for points that suggest
an underlying aetiology or associated structural disease, e.g. history
of rheumatic fever, history of thyroid disease/shunts/chronic liver
disease/pregnancy (associated with flow murmurs), previous MI,
history of congenital disease/syndrome (valve stenosis and
endocardial cushion defects), dizziness/syncope (LV outflow
obstruction), angina (associated with aortic stenosis).
Investigations
A transthoracic echocardiogram is clearly the single most important
investigation, but other investigations are useful, e.g. ECG for cardiac
rhythm (e.g. atrial fibrillation associated with mitral disease; LVH
associated with aortic stenosis), and CXR (heart size and aortic
contour).
Palpitations
Ask how well tolerated the palpitations are, as this factor will be
very important to the patient. Other useful points in the history:
Ask for the nature of the palpitation (pauses and thumbs suggest
extra-systoles with compensatory pauses), irregular or regular
(irregular palpitation suggests atrial fibrillation or frequent
extrasystoles).
Ask the patient to tap out the rhythm on the desk (a slow forceful
rhythm suggests bradycardia or bigeminy rhythm with
compensatory pauses.
Does the patient experience palpitations as fast or slow? Simple
ectopics are usually easy to determine from the history alone:
Patients refer to missed or extra beats. Sudden bursts of
fluttering may indicate paroxysmal atrial fibrillation. A clear onset
and offset to rapid regular palpitations is characteristic of re-entrant
tachycardias.
Ask about associated symptoms especially chest pain, dyspnoea,
faintness (this strengthens the argument for pacemaker
implantation with bradycardias), anxiety, tremor, increased

appetite. Palpitations accompanied by diarrhoea, wheezing and
flushing may be indicative of carcinoid syndrome.
Ask also about psychiatric syndromes, e.g. panic attacks,
generalised anxiety disorder, depression, somatization.
How long ago did the palpitations start? How frequent are they?
Triggering factors (e.g. exertion in VT, posture for vasovagal
syndrome, emotional stress, often sinus tachycardia, effect of
exercise i.e. patient may notice that extrasystoles disappear during
exercise, alcohol for atrial fibrillation, and caffeine which has a
questionable relationship to extrasystoles).
Previous medical history: Fever, anaemia, previous history of heart
disease (risk factors, previous events), hypertension (most recent blood
pressure), mitral valve disease (previous rheumatic fever) or thyroid
disorders, phaeochromocytoma, hypoglycaemia, mastocytosis.
Elicit a full drug history, consider beliefs concerns and expectations,
and a social and occupational history.
Investigations
ECG, 24-HT, CXR, echocardiogram, bloods, Respiratory System.
Asthma
Questions relating to current symptoms: Onset and duration of
symptoms, nature of symptoms (cough, sputum, haemoptysis,
worsening wheeze, fever, chest pain, disturbance of sleep, presence
of nocturnal cough); any diurnal variation; precipitating factors
infection, contact with known allergens, stress, exercise, poor
compliance with medication; how the PEFR has changed.
Questions relating to where the diagnosis was made, underlying
stability/severity of disease, reversibility associated with therapy;
usual treatment home nebulisers, steroids; previous exacerbations
and their management (?whether in hospital); days taken off work;
previous admissions to ITU and whether he was ventilated in the
past; primary or secondary care of management.
Previous medical history: Eczema, atopy, nasal polyps, recent
surgery.
Drug history: NSAIDs, -blockers, common allergies (including drug
allergies).
Travel history: Recent air travel (?are the symptoms actually
suggestive of a pulmonary embolus).
65
Social history: Anxiety and stress, smoking. Family history: Asthma,

clotting disorders.
Investigations
PEFR, pulse oximeter, arterial blood gases, CXR, FBC, U&E, CRP and
ESR, sputum MC+S, spiral CT scan, lung funtion tests, serum
precipitins.
Management
As well as medication for asthma, the patient should ideally stop
smoking and avoid any relevant allergens. Admit if: Hypoxic, PEFR
< 50% of patients normal value; patients with severe attacks requiring
urgent reatment and early liaison with ITU, patients with a history of
brittle asthma should be admitted even if the symptoms are mild.
Follow the BTS guidelines (see Station 1 section).
Breathlessness/Dyspnoea
Points in the history Assessment of the premorbid state.
Account of symptoms (acute or chronic/progressive; sudden or
insidious; episodic, stepwise or continuous?).
Could the breathlessness be due to a cardiac complaint as well as
a respiratory one? (Is the patient on a medication for chronic heart
failure?)
Is the breathlessness progressive as in lung fibrosis, COPD or does
it follow a daily rhythm such as in asthma?
Is the breathlessness of rapid onset (e.g. foreign body, anaphylaxis,
anxiety, pneumothorax or pulmonary embolism, where the pain
can be localised and worse on inspiration)?
Does the breathlessness come on over a few minutes or hours? (if
the onset lasts a few hours, consider asthma, COPD, chest infection,
metabolic acidosis, or left heart failure; asthma is distinguished by
the absence of a history of chest pain, the absence of murmurs,
and a previous history of asthma);
Is there a history of antecedent illness? (e.g. pericardial
tamponade);
Is there breathlessness sufficient to wake the patient at night time,
for example, paroxysmal nocturnal dyspnoea, or noctural asthma?;
Does the breathlessness come on over several weeks? (diffuse
pulmonary fibrosis, chronic heart failure, recurrent pulmonary
embolism, anaemia);

Is there dyspnoea at rest or exertion?
Any difficulty sleeping because of symptoms? Usual symptoms
during the day? Effects on daily activities? Effects of daily activities
on symptoms? Concerns about illness?
What is the impact of the disease, both physical and psychosocial?
Enquire about risk factors Past respiratory disease (recurrent
pneumonias, TB), family history, smoking, hypertension, lipid profile,
diabetes, atopy; number of exacerbations per year.
Enquire abour relevant triggers, including exercise, cold, smoking,
occupational exposure (e.g. asbestos, compost), allergens (house dust
mite, dog allergen, cat allergen, birds including parrots, pollen and
moulds). Ask about any evidence of winter exacerbations (e.g. COPD).
Take a decent drug history (especially NSAIDs for wheeze, ACE
for cough, drug-induced fibrosis, e.g. nitrofurantoin, busulphan), and
occupational history including asbestos and compost), social history
(passive, pipe and cigarette smoking), travel history (atypical
pneumonias and TB).
Cardiovascular (LV systolic/diastolic failure), LVH, myocardial
ischaemia, pericardial disease; respiratory (COPD, asthma, upper
respiratory tract obstruction, interstitial lung disease, respiratory
infection, pleural effusion), other (anaemia, diabetic ketoacidosis,
salicylate poisoning, hyperventilation syndrome). Features of a
hyperventilation syndrome include headaches, dizziness, palpitations
and peioral paraesthesia.
Investigations
These might include:
Chest X-ray (emphysema, asthma, consolidation, cardiac failure,
pulmonary oedema, pneumothorax, bronchial carcinoma),
FBC (to exclude anaemia, or polycythaemia),
ECG (arrhythmias),
PEFR,
Full lung function tests including spirometry, reversibility of forced
expiratory volume in 1s, arteral blood gases (severity of disease
and type of respiratory failure),
Sputum and blood cultures should be taken if an infective aetiology
is suspected. Blood immunological investigations (if relevant),
Bronchoscopy can be performed if a foreign body is aspirated. CT
of thorax can evaluate masses of unknown aetiology,
67
An echocardiogram is useful if cardiac failure or a valvular lesion

is suspected. A V/Q scan or CTPA is useful if pulmonary emboli
are suspected.
Treatment
Consider the following approaches:
Withdrawal of offending agent (e.g. fungus in hypersensitivity
pneumonitis, drug in drug-induced lung fibrosis).
Symptomatic treatment with bronchodilators and anticholinergics,
antibiotics.
Home oxygen therapy and inhaler technique (depends on degree
of hypoxia and blood gases).
Consider also non-pharmacological treatments (e.g. postural
adjustments and breathing exercises to relieve anxiety, fan cooling).
Cough
Features of a good cough history would include the following:
Ask about the duration of symptoms: Patients often put up with a
cough for many years; a morning cough present for many years
productive of white sputum is characteristic of chronic bronchitis;
a longstanding, highly productive cough is suggestive of
bronchiectasis. Is there any diurnal variation?
Ask about the type of cough. For example, with vocal cord paralysis
the cough sounds bovine. Laryngitis, especially in children, leads
to a harsh croupy cough.
Enquire about other respiratory symptoms such as haemoptysis,
postnasal drip (symptoms of sputum running down the back of
the throat, unpleasant, other ENT symptoms).
Enquire about features suggestive of specific diagnosis: E.g.
tuberculosis, asthma, sarcoid rashes, eye symptoms, glandular
enlargement or shortness of breath, allergy.
Is the cough related to meals or lying down? This may be due to
to gastro-oesophageal reflux.
Is the cough related to starting medication? Common examples
include ACE inhibitor, NSAIDs, or amiodarone (which can cause
a pneumonitis).
What is the impact of cough on the patient? You could ask about
the effect on urinary continence and sleep.

Is there a history of smoking? (Itself can cause a chronic cough,
bronchogenic carcinoma and chronic bronchitis) Ask about history
of passive smoking.
Enquire about previous medical history: Childhood asthma, atopy, nasal
polyps, peptic ulcers, ENT surgery or sinus problems.
Ask about family history (asthma/atopy, lung cancer): Living conditions
(overcrowding, damp housing), exposure to pollution. Travel to
endemic areas.
Asthma, cough variant asthma, gastrooesophageal reflux, postnasal
drip, postviral infection, allergy, GORD, ACE inhibitor, bronchitis,
tuberculosis, inhaled foreign body, lung neoplasm, sarcoid, drugs,
psychogenic.
Investigations
FBC (including eosinophilia), CXR (to exclude lung caner, sarcoid and
TB), respiratory function tests, U&E, LFTs, bone profile, allergen
testing, serum ACE, CT sinuses (postnasal drip), PEFR chart,
oesophageal pH monitoring, trial of therapy (particularly important
for cough variant asthma or asthma). Bronchoscopy is not required
unless CXR is abnormal or RFTs show a restrictive defect (will also
require HRCT).
Haemoptysis
Confirm haemoptysis is not a fleck of blood, and is not haematemesis.
Ask therefore about the nature of the haemoptysis fresh-red blood
or mixed in with sputum. If from the mouth, a nasopharyngeal source
is likely. Blood from the chest is usually red, not brown. Any history
of recent trauma such as a sports injury?
When did the haemoptysis develop? How often? What is the
approximate volume eggcup or spoonful (any cause),
Ask about related symptoms suggestive of an underlying disorder:
Pleuritic chest pain, dyspnoea, fever, and recent leg swelling (i.e.
DVT) may suggest a PE. If so, elicit relevant risk factors for PE.
A long history of dyspnoea may be associated with chronic lung
disease or mitral stenosis.
69
Progressive weight loss is suggestive of TB or bronchial carcinoma.

Cough and purulent sputum imply infection; tuberculosis can
present with fever, night sweats, and haemoptysis.
Lung cancer is suggested by lethargy, weight loss,
lymphadenopathy, bone pain and paraneoplastic syndromes.
Vasculitis is suggested by fevers, joint pains, haematuria, rash.
Epistaxis and haemoptysis occur together with Wegeners
granulomatosis and hereditary haemorrhagic telengectasia.
Past history of cardiac or pulmonary (e.g. COPD, pneumonia,
tuberculosis, recurrent infections suggesting bronchiectasis), history
of vasculitis, and specifically any history of rheumatic fever as a child
which may have caused mitral stenosis. Recurrent haemoptysis over
several years is common in bronchiectasis, but consider also TB,
aspergilloma and lung malignancy.
Drug history (anticoagulants), contact history (areas endemic with
TB, air travel), family history (e.g. haemorrhagic telengectasia or a
disorder of coagulation/thrombophilia), smoking history, occupational
history (exposure to asbestosis).
Pneumonia, lung cancer, bronchiectasis, pulmonary emboli, TB,
overanticoagulation, rare causes (arteriovenous malformation,
amyloidosis, sarcoidosis, foreign body, benign tumour, vasculitides,
aspergilloma, mitral stenosis).
Investigations
These should be targetted at what is most likely. Possibilities include:
CXR (lung cancer, COPD, bronchiectasis, TB, pneumonia),
Sputum (cytology if there is a suggestion of bronchial carcinoma,
AFBs in the sputum for TB),
Blood tests (FBC, U/Es, anti-GBM antibodies, LFTs, clotting
screen, cANCA, D-dimers, calcium),
ECG (right heart strain, atrial fibrillation, urinary microscopy for
red cell casts),
Spirometry,
Oxygen saturation,
CT scan of thorax (useful especially for bronchiectasis),
Bronchoscopy (lung cancer; useful also for other sources of bleeding
such as arteriovenous malformations),

Aspirate of pleural effusion, biopsy of any tumour or relevant organ
(e.g. kidney),
Radioisotope scan (e.g. V/Q for pulmonary embolus),
Previous investigations and treatment (e.g. surgical, radiotherapy,
chemotherapy, palliative care),
Echocardiogram (useful for both left and right ventricular failure,
as well as mitral stenosis).
Tuberculosis
Ask first of all about the duration of symptoms and enquire about
specific features is the cough productive, sputum quantity and colour
Is there haemoptysis (see above)?, Is there chest pain often related to
pleurisy?, Is there shortness of breath?, Is there a temperature, Is
there loss of weight
Pulmonary TB: Typically causes a slow onset of symptoms including
productive cough, haemoptysis, weight loss and night sweats.
Neurological TB: Cranial nerve palsies, meningitis, spinal cord
involvement. Rashes, e.g. lupus vulgaris, erythema nodosum. Adrenals
lethargy, anorexia and dizziness. Atypical pneumonias. Sarcoidosis.
Previous medical history: BCG vaccination or recent Mantoux/Heaf test;
immunosuppression HIV, immunosuppressive drugs; other recent
infections, e.g. shingles.
Drug history: Previous treatment for TB. Family history: TB and contacts
with them. Travel history: Especially to areas endemic of TB. Social
history: Occupational, crowded accommodation, contacts, alcohol
dependence syndrome, living rough. Sexual history: HIV/AIDS.
Investigations
Repeat CXR, sputum smear and microscopy, Grams stain, ZiehlNielsen stain, blood cultures, FBC, film haemolysis. LFTs prior to
anti-TB therapy, hepatitis, U&E hyponatraemia, complement fixation
test; HIV test; Mantoux test; serum ACE; sputum culture for TB,
pulmonary function tests; consider pleural biopsy; CT and biopsy.
Management
Triple therapy, side-effects (rifampicinred urine, tears; isoniazid
impaired LFTs, peripheral neuropathy; pyrazinamidearthralgia and
71
sideroblastic anaemia; ethambutoloptic neuritis and peripheral

neuropathy). TB is a notifiable disease. Regular f/u. Rifampicin results
in less effective oral contraception. Treatment plan is triple therapy
with rifampicin, isoniazid, pyrazinamide for 2 months followed by
rifampicin and isoniazid for another 4 months.
Wheeze
Do not forget an elementary history of recent asthma symptoms
including wheeze, cough, dyspnoea, haemoptysis, occupationallyrelated. Do the symptoms improve on holiday (suggestive of
occupational asthma: ask about nature of job)? Ask about exacerbating
factors. You will also need to establish any relationship between
trigger and onset of symptoms (if on first exposure, irritant, if later,
sensitization). Is there a past history of allergy and atopy? Ask about
peak flow meter and readings. Ask about social factors (as for asthma)
and the concerns of patient.
Narrowing of airways (asthma, bronchitis, bronchiectasis, foreign
body, tumour), left ventricular failure, carcinoid syndrome, pulmonary
eosinophilia (e.g. tropical eosinophilia, allergic bronchopulmonary
aspergillosis, polyarteritis nodosa).
Investigations
PEFR diaries and lung function.
Management
Asthma is described above and a complete understanding of the
management of this is expected. Consider an occupational physician
referral, if appropriate. The only effective treatment is avoidance of
the precipitant. Financial problems and difficulty finding work may
be relevant. Finally, consider that employees with occupational asthma
are eligible for industrial injury benefit abdominal system.
Abdominal Swelling
Gaseous distension (malabsorption syndrome), fat (for example,
Cushings syndrome causing fat deposition in the abdominal wall, or

obesity), solid (hepatomegaly, splenomegaly, nephromegaly; if cystic,
consider bladder, pancreatic cyst, ovarian cyst), pregnancy
(amenorrhoea), ascites. Consider specifically cause of ascites: Nonliver causes including generalised fluid retention, e.g. heart failure,
hypoalbuminaemia, constrictive pericarditis, portal or hepatic vein
thrombosis; intraabdominal disorders, hypothyroidism, patients on
haemodialysis, liver failure. If exudative, consider malignancy, and
infection including TB. Drug history: Steroids. Social history: Alcohol
intake.
Investigations
Diagnostic tap of ascites is necessary for cytology, microscopy, AFBs
and amylase. Neutrophil count is useful for diagnosis of bacterial
pericarditis. CT of abdomen is the investigation of choice for an
abdominal malignancy. Abdominal X-ray to confirm gas and fluid
levels, and to examine for abdominal obstruction.
Abnormal Liver Function Tests

Enquire about any constitutional symptoms or episodes of jaundice
(especially with fasting), colour and change of stools and urine, weight
loss, new lumps, and features of haemochromatosis (e.g. appearance,
arthralgia).
Past medical history of liver disease, abdominal surgery, abdominal
pain or gallstones, autoimmune diseases, diarrhoea (associated with
Crohns, ulcerative colitis), previous malignancy (and related
investigations, e.g. smear/mammogram).
Drug history: IV drugs (relevant to hepatitis B and C), herbal remedies,
regular prescriptions, over-the-counter medications, recent blood
transfusions.
Family history: Liver disease, malignancies, autoimmune disease,
Gilberts syndrome.
Social history: Detailed smoking and alcohol history (if there is
suggestive of heavy alcohol abuse, this should be taken further), travel
abroad, unusual foods (shellfish associated with Hepatitis A). Sexual
history: Contraception and Hepatitis B, C, D and HIV risk.
Investigations
LFTs, FBC, viral hepatitis serology, autoimmune profile, serum
electrophoresis, liver ultrasound.
73
Management
Abstention from alcohol (if relevant), treatment aimed at symptoms
and underlying cause (e.g. ursodeoxycholic acid for PBC, steroids for
autoimmune liver disease; venesection and desferrioxamine for
haemochromatosis).
Diarrhoea
In simplest terms, diarrhoea can mean an increase in stool frequency
or stool volume.

There needs to be a detailed description of the diarrhoea itself: This
should ideally include:
The frequency of bowel action and timing,
The volume and consistency (watery/clear/frothy, fluid/brown,
semi-formed, solid),
The presence of blood and slime (melaena is tarry), features of
steatorrhoea (implied by pale and difficult-to-flush stools),
The relationship of bowel actions to eating, and particular foods
(e.g. bread, cakes, oats, etc.)
Any feelings of incomplete evacuation, any accompanying pain,
and tenesmus (the feeling of a need to evacuate when the rectum
is empty),
Alarm symptoms including anaemia, loss of weight, anorexia,
recent onset of progressive symptoms, melaena or haematemesis,
dysphagia, abdominal mass.
If the patient is diabetic, and suffers from nocturnal diarrhoea,
especially consider autonomic neuropathy, and consider antibiotic
prophylaxis and loperamide in the management; but first of all
consider in the history the persons occupation, and also whether
there are associated features of autonomic disturbance such as
impotence or incontinence.
Obtain a chronological description of its onset and events related
to it (the time course, precipitant, exacerbating/relieving factors, other
symptoms), an enquiry into the background factors that might explain
the cause of the diarrhoea or have resulted from it, and finally an
enquiry into related symptoms (particularly if the patent is ill with
weight loss, fever, or symptoms affecting other symptoms).

Enquire about symptoms suggestive of an underlying condition.
Overall, organic pathology is suggested by certain features, for
example, symptoms at night, mouth ulcers and unintentional.
Irritable bowel syndrome is characterized by a flurry of bowel
actions in the early morning but nothing later in the day. There
may be bloating and colicky pain with IBS. The diarrhoea never
occurs at night.
Abrupt onset implies infections or toxins.
There may be features of thyroid disease.
A colonic pathology is suggestive of watery stool often with blood
and mucus, possibly with urgency of defaecation). If symptoms
suggest large bowel disease, look for other features of clinical
syndromes, such as inflammatory bowel disease (eye, mouth ulcers,
abdominal pain, skin and eye involvement, arthritis), colorectal
carcinoma (per rectum bleeding), diverticular disease and superior/
inferior mesenteric ischaemia.
Small intestine diarrhoea is suggested by features of steatorrhoea,
i.e. offensive grossly fatty and difficult to flush stools, often
associated with severe back and abdominal pain or weight loss)
and exocrine pancreatic insufficiency (steatorrhoea and weight
loss). If symptoms suggest small bowel disease, ask about relevant
past medical history thyroid disease, diabetes, surgery; alcohol
intake, medications, e.g. recent medications, and the four
commonest causes of malabsorption in the UK coeliac disease
(dermatitis herpetiformis), cystic fibrosis, posteneritis enteropathy
and giardiasis.
Enquire about features of overflow (for example, constipation or
partial bowel obstruction).
Enquire about bleeding through the rectum (spotting and fresh
blood on toilet tissue during or following bowel action is found in
haemorrhoids or fissure; fresh and profuse bleeding is found in
diverticular disease, inflammatory bowel disease, arteriovenous
malformation or carcinoma; dark/altered blood usually from lesions
in the proximal colon; red-current stool is found in intussusception;
mucoid bloody diarrhoea is found in typhoid and amoebiasis).
Previous surgical history: E.g. post-gastrectomy, gut resection.
Previous medical history: Abdominal surgery (bacterial
overgrowth), autoimmune disorders. Social history: Stress and
depression, smoking and alcohol consumption (alcohol is a potent
laxative).
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Drug history: E.g. chemotherapy, alcohol, laxatives/purgatives,

antibiotics, SSRIs, NSAIDs, excessive laxatives or purgatives. Also
enquire about non-prescription medications.
Travel history: Tropical sprue can occur years after travel abroad
(Caribbean and Asia). Other lifestyle issues (e.g. high fibre diet, stress,
living conditions, sexual orientation if AIDS is a concern).
Family history: A family tree should be drawn with details of age
of diagnosis of cancer, age of death, type of malignancy.
Questions Specific to Crohns Disease

Where was the diagnosis made? Any previous investigations
performed (colonoscopy, barium meal/follow through)? Progression
of disease remitting-relapsing, previous surgery. Previous response
to medical treatment. Features of the disease: Associated abnormal
urinary symptoms and change in abdominal size, fevers (disease or
abscess), lethargy (malabsorption or anaemia associated with Crohns
disease), any abdominal masses (abscess or Crohns mass), the ability
of the patient to eat/drink, non-GI manifestations (eyes, arthropathy,
skin lesions, liver disease). Is there a family history? Social history is
especially important: How does the disease affect her home and
occupational life and is there good family support? Enquire about
smoking as this is thought to exacerbate Crohns disease.
As above. In summary, these include: Irritable bowel syndrome,
inflammatory bowel disease, GI malignancy, infective diarrhoea,
drugs: Laxatives, alcohol history, malabsorption, diverticular disease,
thyrotoxicosis.
Investigations
FBC, ESR, CRP, U&E, LFTs, serum amylase.
Stool faecal fat If very high, consider pancreatic cause and monitor
a response to pancreatic enzyme replacement (there may be
pancreatic insufficiency or inactivation of pancreatic enzymes due
to chronic pancreatitis or gastric acid hypersecretion); if high,
perform endomysial antibodies (if positive, follow response to
gluten-free diet), if these antibodies are negative consider low
duodenal biopsy (e.g. giardia, Whipples disease, amyloid disease,
secondary coeliac syndrome, tropical sprue).
Stool microscopy for infection.

Sigmoidoscopy/colonoscopy.
Ultrasound scan if considered to be a collection.
Further investigations include barium studies for blind-loop
syndrome.
Management
This may include some of the following:
Resuscitate (rehydration and correction of electrolyte imbalances
may be necessary) Correct the underlying cause (e.g. pancreatic
enzyme replacement). Antidiarrhoeal medication (e.g. opioids).
For optimisation of Crohns disease, treat acute pain with analgesia.
Chronic pain relief with opiates can be counterproductive
(constipation).
Optimise
medical
management:
Glucocorticosteroids, aminosalicylates, azathioprine, metronidazole
(for severe perianal involvement), infliximab.
Dysphagia
A good dysphagia history could comprise:
Are symptoms getting progressively worse? Chronic and/or
intermittent pain is more likely due to a benign stricture or achalasia
of the stomach.
Is there pain on swallowing? Usually this is due to oesophagitis;
achalasia where swallowing can provoke pain radiating to the neck;
oesophageal cancer (difficulty in swallowing solids occurs at the
beginning of the meal, but after a few pain-producing mouthfuls,
the rest of the meal passes with relative ease),
Is the dysphagia for solid food (obstructive) or liquids (motility)?
Where does the food get stuck? High dysphagia may suggest a
compression web, pharyngeal pouch, thyroid swelling.
What are the associated symptoms? You might ask about episodes
of vomiting, choking, splutting, past history of regurgitation or
aspiration, haematemesis, heartburn, weight loss, loss of appetite.
Look for features suggestive of an underlying diagnosis:
Anxiety in a young female, for example, suggests a psychogenic
aetiology or globus hystericus.
Food and liquid regurgitated easily on turning the head is
suggestive of a pharyngeal pouch.
Abnormal skin texture and circulatrion in the hands and fingers is
suggestive of systemic sclerosis.
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Parotid gland enlargement, dry eyes and mouth are associated

with Sjogrens syndrome.
Neurological features such as ptosis or fasciculations may prompt
enquiry about myaesthenia or motor neurone disease.
A history of mechanical causes may be elicited such as fish-bones
in the piriform fossa or foreign body).
There may be an inflammatory condition of the mouth (e.g.
leukoplakia, carcinoma of the tongue; there may be a history of
heartburn suggestive of reflux oesophagitis).
A good drug history may give you useful clues (e.g. NSAIDs, K+
or aspirin causing infective oesophagitis by Candida, Herpes, CMV).
Other conditions: Carcinoma of the bronchus, benign oesophageal
stricture. Ask specifically about risk factors for oesophageal carcinoma
(smoking, alcohol excess, possible dietary factors, achalasia of the
cardia, Plummer-Winson syndrome, tylosis).
Differential diagnosis: As above.
Investigations
Relevant blood tests, CXR (for aspiration, foreign body, achalasia,
bronchial Ca), ECG (left atrium hypertrophy), barium swallow
(pharyngeal pouch, achalasia, external compression), upper GI
endoscopy (useful for foreign body, candidiasis, stricture, PlummerVinson syndrome), CT chest (mediastinal nodes, malignancy).
Management
Treat the underlying cause. Management options therefore vary (e.g.
oesophageal dilatation of stricture, surgical excision of tumour and
pouch, palliation with stent, remove foreign body).
Epigastric Pain and Dyspepsia

Site of pain, duration, character/nature, whether the symptoms are
of new onset, progressive, recurrent, episodic or recurrent, constant
or intermittent, radiation to the back or shoulder, precipitating factors
such as movement, effect of food or inspiration, other gastrointestinal
symptoms (e.g. heartburn, vomiting, dysphagia, haematemesis, change
in bowel habit, rectal bleeding, jaundice, pale stools, dark urine, loss
of weight and appetitite, bloating), whether previously treated
including previous GI investigations, haematemesis almost always

needs further investigation, drug history (NSAIDs, codeine,
coproxamol, corticosteroids, aspirin), response to treatment.
Alarm symptoms (anaemia, loss of weight, anorexia, recent onset
of progressive symptoms, melaena or haemaemesis, dysphagia,
abdominal mass), consider the history also of a Mallory-Weiss tear
where the tear results after a bout of severe vomiting.
Take, as usual, a full conventional history. Points to include:
Previous medical history: Cardiac disease, depression, known
history of peptic ulcer diseasse or varisces, chronic liver disease,
familial blood dyscrasia.
Drug history: Precipiting drugsNSAIDs, steroids, anticoagulants,
alcohol; medication to alleviate symptoms.
Family history: Malignancy. Smoking history and alcohol history.
Psychiatric features.
Enquire about occupational history, stress and psychosocial aspects,
alcohol and smoking history, and importantly the patients own
concerns.
Investigations
< 45 years, dyspepsia, lack of alarm symptoms, assess H pylori status
and eradication therapy, otherwise consider endoscopy. British Society
of Gastroenterology guidelines suggest that for first presentation of
dyspepsia that patients < 45 years without alarm symptoms should
have H. pylori serology checked and receive antisecretory treatment,
and patients 44 (or 55 years) or over or patients with alarm symptoms
should be referred for UGI endoscopy. For gastric carcinoma, consider
gastroscopy and biopsy.
There are certain features of ulcers well known to medical students
and rapidly forgotten by junior Physicians. Duodenal ulcer (epigastric
pain occurring before meals, waking them at night, and relieved by
food, milk, alkalis and belching), gastric ulcer (pain usually occurs
after meals, often making the patient afraid to eat and resulting in a
loss of weight; vomiting can relieve the pain), oesophageal reflux,
depression, cardiac pain, gallstones, pancreatitis, carcinoma of the
stomach (acute haemorrhage, epigastric pain, weight loss, important
in the over 60s).
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Investigations
FBC, LFTs, calcium and glucose; Helicobacter antibodies; endoscopy
and CLO testing; ECG if cardiac cause; liver ultrasound. Management:
Stop precipitating factors smoking, stress, alcohol, NSAIDs. If the
patient is depressed, professional follow-up.
Jaundice
Ask first of all where the patient first noticed prodromal illness of
anxiety, fever, or malaise, whether there was any unwellness before
the jaundice, duration, previous episodes, features of cholestasis such
as pruritus (primary biliary cirrhosis), upper abdominal pain
(gallstones), the colour of stools (pale if obstruction is complete), back
pain and fatty stools if pancreatitic involvement, painful jaundice
(alcohol, infection, drug-induced, Wilsons disease, hepatitis, biliary
colic, pancreatitis, cholecystitis, metastatic and Budd-Chiari) or painless
(e.g. hyperbilirubinaemia, Gilberts, pancreatic or biliary malignancy,
haemochromatosis, primary biliary cirrhosis), features of liver failure
(reduced attention span, daytime somnolence), respiratory or cardiac
symptoms.
Full alcohol history and related social factors (including CAGE
questionnaire). Ask also about any recreational drug use or sportsrelated drug use (e.g. anabolic steroids).
Travel history (schisotosomiasis, viral hepatitis, clonorchiasis,
amoebiasis).
Occupational history (hepatitis B or C in health care workers,
leptospirosis, alcoholic liver disease, toxins).
Previous medical history (liver, gallstone history, recent blood
transfusions, other autoimmune disorders in relation to PBC and
CAH), previous surgical history (biliary stricture, retained stones,
hepatic metastases, halothane hepatitis), previous episodes of jaundice
(viral hepatitis, gallstone).
Risk factors for viral hepatitis (recent travel abroad, shellfish
consumption, i/v drug abuse, tattoos, sexual).
Family history (inherited haemolytic anaemias, isolated
hyperbilirubinaemia, haemochromatosis, Wilsons disease, 1 antitrypsin deficiency, contact with hepatitis B or C), drug hepatitis
(paracetamol, antibiotics).
Investigations
This essentially involves a blood hepatitic screen.
If unconjugated hyperbilirubinaemia, look for reticulocytosis
suggestive of a haemolytic anaemia (stools are normal or dark; urine
darkens on standing).
If there is a conjugated hyperbilirubinaemia, and the stools are
normal, then consider possibility of hepatocellular carcinoma. If
conjugated hyperbilirubinaemia, but the stools are pale and urine dark,
it is advisable to perform abdominal ultrasound. If the ultrasound
shows normal intrahepatic bile ducts, consider intrahepatic cholestasis.
If the ultrasound shows dilated intrahepatic ducts, consider
extrahepatic cholestasis.
For rarer causes, consider genetic studies (e.g. haemochromatosis
and Wilsons disease), and also for cause in general a liver biopsy.
Management
This may involve discussion of pathology of alcoholic liver disease,
consequences of alcohol dependence syndrome.
Lower GI Haemorrhage and Melaena

Nature and frequency of blood passed, onset of symptoms, patients
definition of diarrhoea, associated nocturnal diarrhoea (ulcerative
colitis), number of bloody stools per day, abdominal pain/urgency/
tenesmus, straining, constipation and pain (fissure), rectal lumps/
masses, previous GI history (haemorrhoids, bleeding disorders, food
poisoning), drug history (NSAIDs, anticoagulants, iron and bismuth),
alcohol history, FH of GI neoplasia and polyps, concerns of patient
particularly cancer. Systemic features such as anorexia and malaria.
Colonic cancer, ulcerative colitis.
Investigations
FBC, routine biochemistry, stool microscopy, flexible sigmoidoscopy,
double contrast barium enema, colonoscopy.
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Vomiting
Ask about the following:
Frequency of vomiting.
Relation to any medication (a full drug history is required).
Separate evaluation of the nausea, including whether present before
and after the vomiting, triggering and relieving factor.
Time of day of vomiting (mornings suggest raised intracranial
pressure).
Is there any acid brought up?
Enquire about associated clinical features:
Chemical causes (e.g. digoxin, opioids, uraemia) where nausea tends
to be severe and persistent and vomiting produces little or shortlived relief from the vomiting.
Toxins (e.g. alcohol excess).
Other GI symptoms present, but where vomiting predominates
(e.g. constipation, acid regurgitation, dysphagia, abdominal pain,
dyspepsia, bloating, fullness, intestinal obstruction, diarrhoea,
haematemesis and melaena), features of hepatitis (abdominal pain,
biliary pain, itching and dark urine).
Past history of gastrointestinal disorders, e.g. reflux oesophagitis,
pancreatitis or endocrine disorders, psychiatric disorder (e.g. eating
disorders, anxiety).
Neurological features (raised intracranial pressure, visual field loss
optic chiasm compression, acute labyrinthitis).
Ophthalmological features (acute angle closure glaucoma).
Endocrine disorders should be considered, for example,
hypothyroidism (constipation, poor memory, depression, headache
typically with diurnal variation intracranial causes), features of
adrenal insufficiency (e.g. weight loss, depression, nausea/
vomiting, abdominal pain, syncope from postural hypotension),
diabetic ketoacidosis, hyperglycaemia, uraemia.
Pregnancy.
Differential Diagnosis: These are suggested above.
Investigations: Again, as above.
Management: First, correct reversible causes (e.g. remove iatrogenic
drug causes, treat hypercalcaemia). Secondly, consider drug treatments

(e.g. metoclopramide, side effects: Gastric stasis and bowel disorder;
cyclizine: Mechanical bowel obstruction, dystonia). Principles are start
with a first-line drug, re-evaluate regularly.
NEUROLOGICAL SYSTEM
Back Pain
Back pain can be due to a problem in the back or any other predisposing
conditions that impact upon the back, i.e. prostate, carcinoma of the
lung, infection, etc.
Important aspects of the history concerning the back pain include:
Nature, onset (sudden implies trauma-related or disc lesions) or
gradual (degenerative disease), radiation, frequency, precipitating and
relieving factors (e.g. symptoms worse on movement suggests a
mechanical cause), other pains (claudication or neck pain), severe and
unrelenting symptoms suggestive of neoplasia, pathological fractures
(consider myeloma), trauma, impact of pain on life, any involvement
of bladder or bowel function, drug history, smoking history, any
history of a primary neoplasm. Ask about other symptoms (e.g.
infection may be elucidated through a history of night sweats and
fever; osteomyelitis may occur in diabetes and the
immunocompromised).
Red flags for sinister back pain include:
Age > 55,
Non-mechanical back pain with no clear aggravation by movement
or change in posture,
Thoracic pain,
Past history of carcinoma esp. colorectal, breast, renal, thyroid,
Past drug history including repeat prescriptions for corticosteroids
and neurological symptoms or signs.
Other important points include:
Violent trauma,
Alternating/bilateral sciatic,
Weak legs,
Weight loss,
Progressive continuous non-mechanical pain,
Systemically unwell,
Localized bony tenderness,
83
Spine movement in all directions painful,

CNS deficit at more than one root level, bilateral signs of nerve
root tension.
Features of a osteoporosis history: (1) Past family history of osteoporosis,
(2) Psychosocial factors, (3) Risk factors for osteoporosis (e.g. heavy
alcohol consumption, early menopause, hypogonadism, endocrine
disease such as thyrotoxicosis, prolonged steroid use, immobility,
severe chronic illness or malnutrition).
Differential diagnosis: Causes vary across age groups.
For all age groups, consider trauma/fractures, strenuous activity.
Younger patients (<40 years): Prolapsed disc, ankylosing
spondylitis, spondylolisthesis
Older patients (>40 years): Osteoarthritis, spinal stenosis and spinal
claudication, osteoporosis, Pagets disease of bone, herpes zoster.
Other causes include vertebral fractures, TB, metastases, Cushings
disease, psychosomatic, peptic ulcer, pancreatitis, pancreatic Ca,
rectal Ca, abdominal aneurysm, renal Ca. Consider also
gynaecological causes (e.g. uterine tumours, PID, endometriosis).
Investigations: These are targetted at investigating the underlying cause,
and include:
Bloods (including full blood count, liver function tests, serum
immunoglobulins, serum calcium (raised in malignancy, myeloma
and bony metastases), bone profile, parathyroid hormone level,
PSA, Bence Jones protein),
Imaging (X-rays). Spine X-ray is useful for trauma (fractures),
osteoarthritis (narrowed disc spaces and osteophytes), chronic
osteomyelitis (erosion of joint surfaces and destruction of bone),
myeloma (punched out lesions), ankylosing spondylitis (bamboo
spine), secondary depositis (osteolytic or osteosclerotic for
prostate), Pagets disease (sclerotic white vertebrae). Clinical
indications for bone densitometry include personal history of low
trauma, X-ray evidence of osteopenia or vertebral collapse,
maternal history of hip fracture, low BMI, corticosteroid treatment,
oestrogen deficiency, and conditions predisposing to secondary
osteoporosis, including malabsorptive syndromes, organ
transplantation, eating disorders, chronic renal failure, primary
hyperparathyroidism, hyperthyroidism, Cushings syndrome,
prolonged immbolisation, male hypogonadism. A Chest X-ray is
useful for looking for a primary tumour.

Also
MRI (location of a disc lesion, spinal tumour, spinal compression).
Ultrasound abdomen for aortic aneurysm and renal lesions. CT
scan (pancreatic lesions).
Management
General management of back pain includes pain relief, physiotherapy
or bed rest. Correct any infection either medically or surgically (if
there is an abscess). Surgical microdistectomy is a potential option for
a prolapsed disc. Treatment options for osteoporosis include
bisphosphonates, SERMs, HRT, calcium and vitamin D3
supplementation.
Dizziness and Funny Turns

Symptoms including:
Frequency and timing of episodes,
Detailed description of what was observed by the patient (and
others) before, during and after the attacks,
Any associated fall,
Any associated loss of consciousness,
Any associated symptoms and their duration,
Is dizziness precipitated by movements of the head (BPPV,
labrynthitis, head injuries),
Features of hypoglycaemia (nausea, vomiting, tinnitus, palpitations,
aura, hunger, blurred vision, light-headedness, sweating), and
possible causes of hypoglycaemia (e.g. endocrine, mesenchymal/
sarcomatous tumours and hepatic disease, relief of symptoms when
glucose is raised again),
Features of adult onset epilepsy (previous birth trauma or head
injury, symptoms of space-occupying lesion such as headaches, past
history of hypertension, alcohol intake. Ask about tongue biting
and loss of sphincter control).
Features of imbalance (Vertigo: An illusion of movement often
rotatory of the patient and of his surroundings).
Dizziness + vertigo may suggest possible causes:
Benign positional vertigo where there are recurrent acute episodes
of vertigo in response to head movement, worse in the morning,
very short-lived, often associated with cervical spondylosis),
85
Menieres disease (unilateral deafness is usually the first symptom

accompanying tinnitus),
Vestibular nerve damage for example ototoxicity, vestibular
neuronitis, acoustic neuromas, brainstem pathology (e.g. ischaemia,
demyelination, infarction), cerebellopontine tumours, epilepsy.
Vertebrobasilar ischaemia causes dizziness and limb weakness, loss
of vision, diplopia, ataxia, perioral numbness and dysarthria.
Dizziness without vertigo:
Hypotension,
Anaemia (ask about any bleeding),
Cardiac arrhythmia (ask about palpitations),
Endocrine (myxoedema),
Systemic infection,
Psychological (anxiety, ask about hyperventilation),
Carotid artery stenosis,
Tumour of the cerebellopontine angle,
Carotid sinus hypersensitivity (elderly, moving neck, hanging
washing),
Vasovagal syncope which is provoked by emotion, pain, fear or
standing two long and is due to reflex bradycardia with/without
peripheral vasodilatation, TIAs).
Drug history including recreational drugs insulin regimen for
diabetics, home monitoring, diet, use of snacks, -blockers, diuretics
and other antihypertensives. Also enquire specifically about ototoxic
drugs (aminoglycosides and frusemide).
Social history (e.g. whether the patient lives alone, whether he
would like an emergency lifeline system, steepness of stairs if dizzy,
shift-pattern of work), alcohol and smoking, factitious overdosing of
drugs, fear of family.
Blood tests, including glucose, LFTs, U&E, bone function tests, resting
ECG, 24 hour tape, blood pressure, carotid Doppler ultrasound, CT,
EEG, audiometry (loudness recruitment is impaired in Menieres
disease, neuronitis). Realistic goals, e.g. about glycaemia, insulin qds
or rapidly acting insulin analogues for hypoglycaemia, lifestyle
changes.
Investigations: Hb, WCC (infection), 24-hour ECG, Carotid Dopplers,
CT and MRI.
Double Vision
Particular points to note in the history include:
When first noticed, direction, associated ptosis,
Any squint (convergent, concomitant, incomitant): Consider the
causes of a neurogenic squint (IIIrd due to severe trauma, posterior
communicating artery aneurysm or diabetes; IVth due to birth
trauma, trauma, hypertension and diabetes; and VIth nerve palsy).
Other symptoms including tiredness, weakness and fatiguability,
weakness of other groups (e.g. snarl, dysphagia, dysarthria),
respiratory muscle weakness.
Past history of autoimmune disorders, features suggestive of
neoplasm.
Drug history (e.g. D-penicillamine, aminoglycosides for myasthenia
gravis).
Impact of symptoms on patient.
Monocular (originates from cornea or lens, e.g. cataract), or binocular
(cranial nerve palsies (III, IV, VI), internuclear ophthalmoplegia,
extraocular muscle disease (dysthyroid eye disease, myasthenia gravis,
ocular myopathy, ocular myositis), orbital fracture).
Investigations
Anti-AChR assay, Tensilon test, LEMS, hyperthyroidism, botulism,
intracranial mass lesions, thymectomy.
Headache
A common scenario.

A
good headache history should include:

Location (i.e. is it facial or headache pain) and radiation,
Any prodromal symptoms,
Associate symptoms (including signs of meningism),
How recently did the attacks begin and have they changed over
time,
Frequency of attacks (episodic or unremitting) [a headache diary
is often useful] details about the onset (presence of aura, time of
day, associated sleep disturbance, after intercourse or exertion),
associated symptoms, relevant psychosocial details.
87
The duration of each headache, character and intensity, location

of pain and radiation, whether constant or intermittent, does the
pain wake the patient up?
Particular triggers (for migraine, relaxation after stress, missing
meals, missing sleep, long distance travel, alcohol, cheese, chocolate,
caffeine, citrus fruit, sudden unaccustomed exercise); problems with
teeth, sinuses, ear herpetic neuralgia, temporomandibular arthritis,
temporal arteritis), nose sinus infection worse with coughing or
sneezing, eye acute glaucoma, temporal arteritis.
Relieving factors including dark rooms, family history of headache,
what does the patient do during the headache?, investigations and
treatments from the past, and the state of health in between attacks.
Symptoms suggestive of depression or anxiety.
Broadly speaking, the causes are of an acute or chronic headache.
An acute single episode may be a feature of meningitis, encephalitis,
tropical illness, subarachnoid, sinusitis or head injury. Acute
recurrent attacks include migraine, cluster headache, and glaucoma
(mostly elderly long-sighted people with markedly reduced vision
in the affected eye, nausea and vomiting. Attacks may be
precipitated by sitting in the dark).
A chronic headache may be due to tension headache, cluster
headache, migraine, idiopathic intracranial hypertension, or
analgesia overuse. Other causes include neck spondylitis (check if
movement of the neck exacerbates the headache), sinus disease
(ask about localized tenderness/fever), nitrate-induced (after spray
or taking medication), carbon monoxide poisoning (consider if
several members of the family are unwell), and raised intracranial
pressure (typically worse on coughing/straining). Consider also
trigeminal neuralgia (paroxysms of intensive, stabbing pain lasting
seconds, in the trigeminal nerve distribution. The face may screw
up with pain. Pain can recur many times during the day and night).
Management
According to the type of headache, e.g. tryptan or -blocker (+
amitryptiline or pizotifen) for migraine (a triptan should be avoided
if the patient is already taking ergotamine prophylaxis), lithium for
prevention of cluster headaches; tension headaches normally managed
with paracetamol. Urgent treatment is required for serious headaches
include intracranial tumours (symptoms of raised intracranial pressure,

e.g. morning headaches exacerbated by coughing), meningitis (fever,
neck stiffness, altered consciousness), temporal arteritis (> 50 years,
scalp tenderness), primary open angle (acute) glaucoma, idiopathic
intracranial hypertension, subacute carbon monoxide poisoning.
Pins and Needles

Duration, hand/fingers, pain, numbness, clumsiness, feeling of
heaviness, tingling, associated symptoms (tremor, muscle wasting,
paraesthesia), previous medical history including metabolic disorders
such as diabetes and vascular disease, history of trauma, drug history
including isoniazid and nitrofurantoin, alcohol history, dietary history
(B1, B6 and B12 deficiencies), features specifically concerning carpal
tunnel syndrome (hypothyroidism, acromegality, hypothyroidism,
obesity, arthritis, repetitive strain injury, previous fractures, vibrating
tools), concerns of patient.
Peripheral neuropathy, peripheral nerve entrapment/compression
(e.g. cervical rib, carpal tunnel syndrome, disc herniation), spinal cord
disease (e.g. cord/nerve root compression, multiple sclerosis), cortical
or thalamic lesions, hypocalcaemia (e.g. in respiratory alkalosis,
hypomagnesaemia).
Investigations
NCS (sensory nerve action potentials), EMG for denervation.
Management
Treat underlying cause, nighttime splints, local steroid injections,
surgical decompression.
Tremor
Time of onset of tremor, arms/hands, laterality, worse at rest or
posture or intentional, examples of difficulty and type of disability
produced, head nodding, blepharospasm, symptoms suggestive of
Parkinsons disease, neurological changes, history of TIAs, drug
medication (e.g. phenothiazines), alcohol effects (relief of tremor),
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symptoms suggestive of a thyrotoxic state (heat intolerance,

oligomenorrhoea, eye problems, skin rashes), ingestion of xanthines
(e.g. coffee, anti-asthmatics), family history.
Investigations
Neurology, e.g. CT, EEG or MRI, endocrine (e.g. thyroid), psychiatry
(anxiety, dementia).
Idiopathic Parkinsons disease, benign essential tremor, Parkinsonian
syndromes, physiological and exaggerated physiological tremor
(thyrotoxicosis, alcohol, anxiety), Huntingtons disease, ataxia, cortical
dementias, dystonia, myoclonus.
Management
Treat underlying cause. Reassurance (and counselling to come to terms
with disability), management (multidisciplinary team).
Weak Legs
Duration of symptoms, particularly since last completely well, nature
of any pain (shooting pain typically of radiculopathy). sensory loss,
pattern of weakness, evidence of falls, difficulty in getting out of
chairs, other neurological symptoms (e.g. headache, diplopia, muscle
wasting, sphincter problems, tremor, backache, paraethesia).
Candidates would be expected to identify any pointers suggestive
of cord compression, including an acute onset of weakness with
sphincter disturbance and/or saddle anaesthesia, known history
of lymphoma, breast cancer, choriocarcinoma, primary CNS
tumour.
Consider features also suggestive of multiple sclerosis: previous
transient diplopia, vertigo, oscillopsia, sexual difficulties, or bladder
dysfunction; prior weakness.
Other possibilities include: myopathies (suggestive of Cushings
syndrome, thyrotoxicosis or severe hypothyroidism), neuropathies
(diabetes mellitus, malignancy, GB syndrome), myaesthenia gravis
symptoms worse at the end of the day, ocular symptoms;
intracranial mass lesion; myelitis HIV, vasculitis, thromboembolic
tendencies.

A full medical history should be elicited, including: Diabetes, spinal
injury/trauma, neuromuscular disease, metabolic disorder
(hyperthyroidism, Cushings), TB, rheumatoid arthritis (atlantoaxial
sublaxation), operations thymectomy, diabetes mellitus, neck or
spinal irradiation, STDs (syphilis and HIV). Drug history steroids
(reactivation of TB), warfarin, diuretics diuretic or laxative abuse
can cause hypokalaemia, oral contraceptive pill. Social history: Smoking
and alcohol, occupation and nature of work. A systems review as
part of a general history is essential, to look for evidence of an
underlying neoplasm.
Demyelination, cord compression (extramedullary: Meningioma,
neurofibroma and ependyoma), intramedullar lesion (e.g. glioma),
hysteria, myelitis, myopathies, neuropathies, intracranial mass, sagittal
sinus thrombosis.
Investigations
FBC, U&E, bone profile, LFTs, CXR, MRI, evoked potentials, lumbar
puncture.
Management
Of underlying cause.
ENDOCRINE SYSTEM
Diabetes
A
general history of diabetes includes:

Mode of presentation,
Duration,
Type of diabetes,
Symptoms of hyperglycaemia or hypoglycaemia,
Frequency of admission to hospital,
Level of knowledge of his/her level of contro,
His knowledge of symptoms of complications cardiovascular
(knowledge of cardiac risk factors), renal, eye, foot, autonomic,
sexual, his motivation and education with respect to treatment,
and attendance at annual screening,
Onset of any symptoms, for example, painful feet, lipohypertrophy,
muscle weakness and wasting, backache, impact on life,
91
Social history including smoking, alcohol history, exact meal

patterns, exercise patterns (including sexual activity, if appropriate),
A full drug history.
Consider also other causes of any symptoms offered, such as
peripheral neuropathy, briefly, e.g. alcohol, vitamin deficiencies,
thyrotoxicosis, Addisons disease, pernicious anaemia, myeloma, renal
failure and/or uraemia, carcinoma, infections.
Management
Education about diabetes mainly revolves around its complication,
treatment types and goals, dietary advice, lifestyle advice, foot
care monitoring, self-monitoring of urine and blood sugar,
recognition and management of hypoglycaemia, intercurrent illness
management, support groups such as Diabetes UK and driving:
Patients on hypoglycaemic treatment have a responsibility to
inform the DVLA.
Drug treatments for glycaemic control include insulin (newer longacting insulins have more predictable and sustained absorption
from subcutaneous tissue) with short-acting boluses at mealtimes;
sulponylureas precipitate insulin release and are generally used
for type 2 patients who are not overweight (NB: Hypoglycaemia
is an important side-effect), metformin increases peripheral
sensitivity to insulin and is the drug of first choice for those who
are overweight, thiazolidinediones activate peroxisome
proliferators activated receptor gamma which are contraindicated
in cardiac failure and liver disease. Overall glycaemic control is
best measured by HBA1c measurmenent, and the benefit of good
blood glucose control is 7%.
Treatment of painful diabetic feet includes pain relief, glycaemic
control, TENS/pain relief pain. For vascular problems, emphasise
need for treatment of underlying cause (inc. blood pressure,
glycaemic control), multidisplinary tram, avoidance of infection,
outpatient angiography (angioplasty, bypass), anticoagulation,
temporary footwear, daily inspection of feet, good foot hygiene,
avoidance of walking barefoot, prompt referral if abnormality,
selection of footwear.
Other methods of treatment include metatarsal bone resections to
reduce the risk of high-pressure stresses, and debridement of nonviable tissue to reduce the risk of infection (Lancet 1999; 354;
370-1).
Hypercalcaemia
Elicit relevant symptoms of hypercalcaemia (tiredness, mental
confusion, constipation, malaise, depression, abdominal pain, renal
colic, bony pain), as well as features suggestive of an underlying cause
(e.g. sarcoidosis, peptic ulcer, hyperparathyroidism, thyrotoxicosis,
malignancy bone secondaries from breast and lung, or
haematological malignancy, lymphoma, myeloma). A full history
should also pay attention to a detailed drug history (e.g. vitamin D
analogues, thiazides, lithium), family history (hypocalciuric
hypercalcaemia), immobility, concerns of patient.
Differential diagnosis: As above
Investigations: Serum calcium, ECG short QT.
Management: Treatment with hydration and bisphosphonate. Treat
primary hyperparathyroidism with surgery. Preopoerative
localisation: MRI, radioisotope subtraction scanning and the
management of acute hypercalcaemia.
Hypogonadism
Look for other features of panhypopituitarism: Hyperprolactinaemia
(galactorrhoea, reduced libido, headaches), growth hormone deficiency
(lethargy, weight gain, depression reduced muscle mass, sleepiness),
hypothyroidism.
Primary where serum testosterone is low and FSH/LH may be high
(congenital: Klinefelters, cryptochordism, varicocoele, myotonic
dystrophy; Acquired: Mumps, radiation, alkylating and antineoplastic
agents, trauma, torsion, autoimmune, cirrhosis, chronic renal failure),
or secondary where testosterone is subnormal and FSH/LH are
normal/reduced (Congenital: Kallmans, hypogonadotrophic
hypogonadism, e.g. Prader-Willi, abnormal FSH/LH subunits;
Acquired: Idiopathic, malignant tumours, infiltrative disorders (e.g.
sarcoidosis and Langerhans cell histiocytosis), meningitis, pituitary
apoplexy, trauma, critical illness, glucocorticoid treatment, chronic
narcotic administration).
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Impotence
It is essential to take an adequate sexual history, including stress
performance anxiety, history of morning erections/masturbation,
drugs, trauma, neurological symptoms, claudication (a history of
peripheral vascular disease especially buttock claudication is suggestive
of Leriches syndrome), symptoms of chronic renal failure (nausea,
lethargy, peripheral oedema, dyspnoea, vomiting, hiccups and
convulsions), and psychological history.
Psychological (patients may have morning erections), drugs (alcohol,
anti-depressants, -blockers, cannabis, diuretics, major tranquilizers,
recreational drugs), endocrine disorders (hypogonadism/androgen
deficiency, hyperthyroidism, prolactinomas, acromegaly), neurological
(autonomic neuropathy, e.g. diabetes, uraemia, nerve damage after
bladder neck/prostate surgery, multiple sclerosis), vascular disease
(e.g. atherosclerosis).
Investigations
Endocrine, prolactin, testosterone, sex hormone binding globulin, FH/
LSH, glucose, liver function tests.
Management
Knowledge of treatments and appropriate referral.
Polyuria
Chronological history of the polyuria, actual volume of urine passed
(polyuria should be differentiated from frequency of micturition),
volume of intake and types of fluid, colour of urine, appetite, weight,
cough history), current and past psychiatric history (compulsive water
drinking/psychogenic polydypsia). Attempts should be made to elicit
the specific concerns of the patient.
Look for features of diabetes: Associated infection, lethargy,
balanitis, blurred vision, positive family history and weight loss.
Look for features of hypercalcaemia: E.g. weight loss, polyuria,
abdominal pain, constipation, vomiting. Look for causes of

hypokalaemia: drug history, ACTH-secreting small cell carcinoma of
the bronchus, prolonged diarrhoea.
Consider evidence of infections (TB, meningitis, cerebral abscess)
consider the posssibility of a hypothalamic or pituitary tumour causing
cranial diabetes insipidus, e.g. primary craniopharyngioma,
ependymoma, hypothalamic pituitary glioma. Features of pituitary
dysfunction (galactorrhoea, amenorrhea, hypogonadism, visual field
defects, hypothyroidism, hypoadrenalism). This can result from
severe, blunt, head injuries, cranipharyngiomas, pineal gland tumours,
or as a transient postoperative complication following neurosurgery.
Consider the possibility of a nephrogenic diabetes insipidus (e.g.
drug induced, lithium, glibenclamide) or features of chronic renal
failure such as uraemia.
Features of pregnancy or thyrotoxicosis.
History of diuretic phase of acute renal failure.
Ask abpout therapeutic diuretics, for example used in hypertension
or cardiac failure.
Obtain a detailed medical history: Including previous surgical
procedures, previous radiotherapy, previous vascular events
(haemorrhage, thrombosis), head injury. Obtain a drug history
(including diuretics, as well as nephrotoxic drugs including
aminoglycosides, ciclosporin, NSAIDs and ACE-inhibitors) and
smoking/EtOH history.
Investigations
Blood urine, serum calcium, ACE, chest X-ray (carcinoma of the
bronchus, sarcoid, eosinophilic granuloma), urea and electrolytes (K+
and Ca 2+), MRI scan of head, bronchoscopy (granuloma), early
morning paired plasma and urine osmolalities for cranial DI, water
deprivation test. If the plasma osmolality low, consider compulsive
water drinking and diabetes inspidus. Water deprivation produces
only a small rise in urine osmolality in diabetes inspidus compared to
compulsive water drinking. ADH will produce a concentrated urine
in pituitary diabetes inspidus, no effect in nephrogenic diabetes
insipidus.
Management
Treat the underlying cause.
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Incontinence
Causes
Urinary tract infection: This should always be considered in patients
presenting with urinary incontinence.
Constipation: This may cause urinary incontinence by causing
bladder outlet obstruction or by reducing bladder capacity.
Drug induced diuresis
Poorly controlled Diabetes Mellitus
Renal failure
Excessive fluid Intake
Nocturnal diuresis (this may be due to autonomic dysfunction)
Loss of awareness of bladder filling
Patients with severe dementia and/or psychiatric illness may exhibit
severe behavioural disturbances which include inappropriate
urination, (and defaecation).
Unstable bladder: Patients with bladder instability experience strong
detrusor contractions during bladder filling which may be followed
by involuntary expulsion of urine. This may be preceded by the
sensation or urgency but often no bladder sensation is experienced.
They are common in patients with global cerebral disease, e.g.
dementia, cerebrovascular disease. Patients with autonomic
dysfunction may also exhibit bladder instability.
Urge incontinence is present when the interval between the desire
to urinate and involuntary expulsion of urine is very short. Patients
with urge incontinence usually have an unstable bladder.
Environmental and physical factors may contribute towards urge
incontinence. Immobile patients take longer to reach the toilet,
especially when there are stairs to negotiate (When they reach the
toilet they may be unable to unfasten their clothes quickly enough.
Stress incontinence: The underlying problem in female patients with
stress incontinence is either pelvic floor muscle or urethral sphincter
weakness. Stress leakage occurs with increases in intra-abdominal
pressure as a result of standing or coughing especially when the
bladder is full. Pelvic floor muscle weakness may occur due to
damage of their innervation during childbirth or as result of chronic
straining at stool. Vaginal prolapse may also be present in these
patients. Urethral sphincter weakness may be due to atrophic
urethritis which is often associated with pruritus vulvae and
frequency of micturition. In the elderly, this is usually due to
oestrogen deficiency.
Assessment and Investigation

Rectal and vaginal examination.
MSSU/Urine cytology: Cystoscopy is indicated if haematuria is
present without urinary infection.
Incontinence chart: Keep record chart initially for 48 hours.
Fluid intake (aim for 1500-2000 ml/day).
Urodynamic assessment: In most elderly patients it is possible to
diagnose the cause of incontinence from the history and examination
findings. Urodynamic assessment is indicated when there is
difficulty making precise diagnosis, when treatment has not been
successful or when surgical treatment is being considered.
Pelvic floor muscle assessment.
Management
Review medication and stop offending drug(s) if possible or use
an alternative drug. When diuretic therapy is required a short
acting diuretic with a predictable effect should be used, e.g. loop
diuretic.
Urinary tract infection: Antibiotic medication as indicated from urine
culture sensitivity results.
Constipation: Use laxatives or enemas.
Urge incontinence/unstable bladder.
Environmental adjustment (including commode).
Modifications to clothing, e.g. velcro fastenings.
Anticholinergic drugs: Oxybutynin (3 mg b.d.- 5 mg t.d.s.), for
example, may be used to increase bladder capacity and reduce the
distending volume at which urgency and/or unstable detrusor
contractions occur.
Stress incontinence: Pelvic floor exercise programme and electrical
stimulation of the pelvic floor-techniques for the electrical
stimulation of pelvic floor muscles are being developed to augment
pelvic floor exercises. The main benefits, however, appear to be
due to pelvic floor muscle exercises and until further evidence is
available, electrical stimulation should only be used in a research
setting.
Oestrogen for atrophic vaginitis: Traditionally this has been given in
the form of pessaries or vaginal cream.
Bladder neck repair: This is indicated for patients with stress in
continence who do not respond to the above treatment and are fit
for an anaesthetic.
97
Vaginal ring pessaries to control vaginal prolapse are usually

ineffective in the treatment of stress incontinence.
The treatment of choice for prostatic enlargement is transurethral
prostatectomy)
Nocturnal diuresis: (Autonomic dysfunction) - additional treatment
possibilities include 10 degrees head up tilt at night and possibly
fludrocortisone or antidiuretic hormone (DDAVP) at night for
resistant cases.
Patients with incontinence secondary to dementia should be
managed by toileting at planned regular intervals.
Control aids are used for patients with intractable incontinence
and for selected patients undergoing treatment for their
incontinence, including pads and pants and underpants.
Catheterisation is also a possibility.
Weight Gain
Ask about basic details of weight gain, distribution of weight gain,
recent changes in diet including junk foods, types of physical exercise
undertaken, previous attempts at weight loss. Elicit specifically
symptoms suggestive of Cushings (change in appearance, symptoms
suggestive of hypothyroidism, skin changes, hair growth/acne,
proximal myopathy, depression, amenorrhoea/oligomennorhea, poor
libido, poor sleep, hypertension, diabetes, osteoporosis, bone
fractures), or polycystic ovarian syndrome (menstrual irregularities,
hirsutism, obesity). Obtain also a history of cardiovascular disease
(hypertension, dyslipaemia), cardiac failure (fluid may lead to weight
gain), history of renal failure, a history of snoring (obstructive sleep
apnoea), any history of DVT, gallstones, back pain, previous pregnancy
or anaesthetic complications. A full medical history should also include
a family history, a social history (including alcohol history), a drug
history (especially any intake of steroids). Finally, the candidate should
address the patients own perceptions (particularly effects on selfesteem, expectations of the patient).
Investigations
This should include weight and height measurements, waist
circumference, blood pressure and urinalysis for protein. Other useful
investigations are disptix the urine (+++ glucose in Cushings, protein
+++ in nephrotic syndrome), U&Es,thyroid function ests,

dexamethasone suppression tests and a 24-hour urinary free cortisol
collection, and the possibility of scans (MRI of pituitary, adrenal; u/s
abdomen and pelvis).
Management
Options generally include brisk walking, swimming or cycling,
reduction of fat intake, drug therapy when other therapies have failure,
inhibiting appetite pathways. Selective transphenoidal resection is the
treatment of choice for Cushings disease with low-dose cortisol
replacement post-operatively for up to 12 months.
RHEUMATOLOGICAL SYSTEM
Cold and Painful Fingers
Frequency of attacks, precipitating factors especially the cold, other
associated symptoms including peripheral vascular disease, cervical
spine problems, syringomyelia, carpal tunnel syndrome, trauma
(vibrational injury), medical history (such as -blockers), family history
of Raynauds disease, concerns (incl. job).
Consider features suggestive of secondary causes, e.g. connective
tissue disease, peripheral vascular disease, drug-induced, neurological,
trauma-induced, blood dyscrasias. Smoking cessation, nifedipine.
Idiopathic, occupational (vibrating tools), connective tissue disease
(scleroderma, SLE, Sjogrens syndrome, rheumatoid arthritis,
dermatomyositis), cold agglutinins, cryoglobulinaemia,
macroglobulinaemia (Waldenstroms), cervical rib, drugs (-blockers),
vascular disease.
Management
General measures such as wearing gloves, no long term damage
usually.
Weak or Painful Shoulders

The candidate should identify:
Which joints are affected (and in particular whether the joints are
large joints or small joints)?
99
Which part of the arm is weak (if any)?

Is there any swelling and, if so, what the type of swelling is
(synovial is soft and boggy, bone swelling has little associated
heat and redness, fluctuant swelling is caused by fluid and may
feel hot, but is not compressible)?
How long the swelling has been present?
Is the swelling associated with radiation, morning stiffness, skin
rash, nodules, sensory loss. Is there joint stiffness as well as pain?
Stiffness is the inability to get the joints moving again after a period
of rest. The length of time that stiffness lasts is related to the
severity of the inflammation. Morning stiffness improving with
exercise is typical of inflammatory arthropathy. Typically, these
symptoms improve as the day progresses. Pain that gets worse
during the day is likely to be due to degenerative change.
Further questions could elucidate the following:
Enquire about symptoms relating to systemic disorders (e.g.
malaise, fatigue, fever, headache, tenderness of scalp, eye changes,
respiratory and neurological changes).
Enquire about occupational factors (trauma, repetitive strain).
Ask about functional disability, e.g. lifting cups, doing up buttons,
writing.
Enquire about symptoms suggestive of particular underlying
disease. A history of rheumatoid disease might symmetrical
arthropathy in both hands, morning stiffness > 1 hour, various
joints are affected, nodules). For SLE enquire about rashes, sunlight
sensitivity, mouth ulcers, features of Raynauds phenomenon, chest
pains, seizures or depression. Cervical myelopathy (head movement
restriction, pain along the distribution of the dermatomes in the
arms, wasting of the small muscles of the hands). Associated
neurological symptoms (e.g. headache, blurred vision, dysphasia,
dysphagia, loss of consciousness, vomiting, seizure, confusion).
History of hypothyroidism.
Enquire about if there is deformity which is often the end result of
an arthritic process. Disability is frequently also a result, and
ascertain how much the disease interferes with his/her life. The
sort of questions you will need to ask depend on the patients
daily activity and whether he/she can carry out their normal job.
Past medical history (e.g. palpitations, connective tissue, vasculitis,
autoimmune disorders, infections, GI, skin).
Drug history (e.g. thiazides precipitating gout, long-term steroid
use, procainamide, hydralazine).

Social history (smoking, alcohol history, domestic circumstances
including characteristics of house, including stairs, access to front
door, toilet, kitchen facilities).
Muscles: Polymyalgia rheumatica, fibromyalgia, polymyositis,
myopathy, myeloma, drug-induced; Joints: Rheumatoid arthritis,
seronegative arthropathies, osteoarthrosis.
Investigations
Bloods, serology, X-rays, imaging, physiotherapy, ESR,
immunoglobulins, muscle enzymes, EMG/biopsy for a muscle
disorder. If the history is suggestive of TIAs, full investigation includes
24HT, carotid artery Doppler and CT head. Anticoagulation may be
necessary. Patients < 65, consider aspirin. Patients > 75 consider
warfarin if not contraindicated. Treatment of rheumatoid disease may
be relevant, including the use of methotrexate, infliximab and
symptomatic relief by COX-2 inhibitors.
GENERAL
Collapse and Loss of Conciousness
Diagnosis here is reliant important upon a good history.
Firstly, distinguish between dysfunction of the central nervous
system and a mechanical fall.
Secondly, distinguish between the two main types of brain
dysfunction: Syncope (transient reduction of blood flow) and
epilepsy. Consider the common causes of syncope. Postural
hypotension falls after standing up. Cough syncope in chronic
bronchitis and emphysema. Micturition syncope usually elderly
men who pass urine standing up. Carotid sinus hypersensitivity
turning head, syncope with tight colours.
Thirdly, consider other causes such as metabolic disturbance
(hypoglycaemia, drug effect, intoxication).
An adequate history of collapse should include attempts to:
Find out the circumstances in which the collapse happened,
Any prodromal symptoms,
Whether the patient lost consciousness,
History Taking (Station 2) 101
The last thing they remember doing,

The next thing they remember,
How they felt during the attack,
Whether they bit their tongue, became incontinent, or became stiff
and shaking,
Any other attacks and their similarity to the present one, and
relevant risk factors.
The presence of warning symptoms are important (e.g. light
headnessness, chest discomfort, palpitations, dyspnoea suggest a
cardiovascular aetiology; headache, confusion, hyperexcitability,
olfactory hallucination and aura suggest a neurogenic aetiology)
The identification of precipitants such as exertion (e.g. aortic
stenosis, HOCM or exercise-induced arrhythmia), standing
(orthostatic hypotension, vasovagal syncope), cough/micturition
(decreased vasomotor response) or neck extension (vertebrobasilar
insufficiency).
Consider Particular Causes

A history of sudden, transient loss of consciousness suggests a
global problem such as a seizure. Is there any prone to sleep (e.g.
narcolepsy)?
Any evidence of anxiety? (Panic attacks may precipitate vaso-vagal
syncope).
Any loss of memory during an attack? (Transient global amnesia).
Abnormal illness behaviour? (Munchhausens syndrome).
In adult onset epilepsy, care must be taken to search for and exclude
a structural pathology, i.e. mass lesion, neoplasm, bleed, infection,
inflammation). Look for localizing features motor, sensory or
cerebellar symptoms, personality change, diplopia resulting from
a sixth or third cranial nerve palsy. The candidate should establish
risk factors of epilepsy by actively asking about any history of
previous head injury or birth trauma, symptoms of cerebral space
occupying lesion such as headaches, past history of hypertension,
alcohol intake.
A quick recovery is usual after cardiac syncope, although nausea
and malaise may last a few minutes after vasovagal attacks.
Consider relatioship to food, and in particular, hypoglycaemia
(Diabetes, liver disease, hypopituitarism, hypoadrenalism, insulin/
sulphonylurea treatment, reactive hypoglycaemia after a meal,
thyrotoxicosis, post-gastrectomy). Prolonged recovery time (> 5

minutes) with drowsiness, headache and focal neurological signs
suggest neurogenic syncope. Loss of consciousness is highly
unusual in TIA, except in a small number of cases of vertebrobasilar
TIA.
A full medical history should include previous medical history,
drug history (sedatives, hypnotics, hypotensives) and social history
(e.g. flashing lights, illicit drugs, risk factors of HIV, occupation).
Travel history: E.g. histoplasmosis.
Investigations
Investigations should be guided by the history and examination and
include:
Bloods including blood glucose during an attack, GGT, calcium,
liver function tests, serum and urinary toxicology screens, HBA1C,
24 hour ECG if symptoms are frequent and may be required if the
ECG is non-diagnostic (usually the indication for a permanent
pacemaker is so compelling, it may add little information).
Echocardiogram for structural heart disease, ECG (to see previous
MI, LVH, sick-sinus syndrome, heart block, atrial fibrillation).
CXR (calcification in the cardiac silhouette, especially if focussed
around the aortic valve; cardiomegaly and pulmonary plethora).
Tilt testing is used for diagnosing vasovagal syncope (studing the
haemodynamic response to prolonged upright posture).
Imaging including CT head.
EEG (with photic stimulation, sleep deprivation and
hyperventilation), thyroid function. Measure lying and standing
BPs.
If neural infection suspected, lumbar puncture (also useful for
subarachnoid haemorrhage), HIV test, Mantoux test, Toxoplasma
serology, serum ACE.
Management
Treat the underlying cause. A detailed social history and premorbid
condition are essential to determine subsequent management. Consider
loose flooring at home. Alcohol. Driving issues.
FALLS
There is an increasing incidence of falls with age. Approximately 25%
of 70-years-olds experiencing at least one fall per year rising to 35%
in the over 75s. In the over 65s falls are the sixth commonest cause of,

and account for 5% of all deaths. Although only 5% of falls result in
fractures and 5% soft tissue injuries, the remaining 90% may result in
loss of confidence. Causes of falls can be summarised as:
Impaired balance due to ageing
Environmental factors
Medical factors.
Medical factors can be divided into non-specific illness and specific
diseases.
Neurological and vision: Confusion (acute and chronic),
cerebrovascular disease, Parkinsonism, epilepsy, visual impairment,
vertigo.
Drugs: Alcohol, drug-induced Parkinsonism, drug-induced
hypotension/postural hypotension (e.g. GTN, phenothiazines,
prazosin), drug-induced electrolyte disturbance (e.g.
hyponatraemia, hypokalaemia).
Cardiovascular: Postural hypotension, arrhythmias, aortic stenosis.
Other causes of syncope: Micturition, cough, vaso-vagal, carotid sinus
syndrome.
Locomotor: Arthritis, muscle weakness/myopathy, foot problems,
and footwear.
Management
It is essential to take a good history, particularly with regard to loss
of consciousness, position or activity at the time of the fall and specific
symptoms such as chest pain. It is important to know how long the
patient was on the floor and, if possible, to obtain an eye-witness
account. Full examination with particular reference to lying and
standing blood pressure, any neurological disorders, vision and gait
should be performed. Investigation is guided by history and
examination. All identifiable causes such as polypharmacy or untreated
Parkinsons disease should be treated. Rehabilitation and the
multidisciplinary approach will not only restore confidence but also
increase stability and ensure safety if falls occur. A home visit is
mandatory when patients present with recurrent falls and will identify
environmental risks and help provide a safe environment for the
patient.
Discussion
There are a number of important reasons why the elderly are
susceptible to falls. Maintenance of man in an erect posture requires

balancing a large mass over a very small base. Mechanisms involved
include ocular, vestibular and proprioceptive receptors. The whole
process is initially learned in childhood. Under normal circumstances
the body sways from a fixed point with women having a greater
sway than men. Sway also increases with normal ageing.
Ocular mechanisms: We all require visual clues to help prevent falls.
In the elderly, both visual acuity and the threshold for light
stimulation is reduced. This coupled with poor environmental
lighting increases the likelihood of falls.
Vestibular mechanisms: The vestibule is involved with rotatory
movements of the head. These mechanisms become relatively
inefficient as patients age.
Proprioceptive mechanisms: The main receptors are situated in the
cervical interfacetal joints in the neck. Impulses generated in the
neck are coordinated in the cerebellum with the efferent pathway
being via the medial longitudinal fasciculus. Cervical spondylosis
or the wearing of a cervical collar renders these receptors
inefficient. Additionally, vascular problems in the carotid may lead
to balance disturbances.
Confusion or Personality Change

Dealing with a confused patient may also be the focus of a
Communications Skills and Ethics station.

A collaborative history from relatives is paramount.
Find out when the symptoms were first noted, the degree of the
patients insight, orientation in time and place, behavioural
problems (personality, mood, sleep, concentration, disorientation),
differences in thinking (slow and muddled, problems in memory),
differences in perception (delusions or hallucinations), speech,
features of depression, personal hygiene.
A medical history should try to identify any endocrine disorder
(diabetes, thyroid disorders), history of malignancy (cerebral
metastasis or hypercalcaemia of malignancy), history of trauma,
seizures, vascular symptoms, (anti-convulsant therapy or nonconvulsive status).
A full drug history is vital in a patient with confusion especially to
look for any compliance issues or any inadvertent overdose, e.g.
benzodiazepines, barbiturates. Ask also about any intake of illicit
drugs.

A social history with risk assessment (e.g. gas) is needed, including
the impact of the patients symptoms on family. Also relevant is
previous chronic exposure to carbon monoxide, excessive alcohol
intake.
Drugs (opiates, anticonvulsants, L-dopa, sedatives, recreational),
alcohol withdrawal, metabolic (hypoglycaemia, uraemia, liver failure,
anaemia), hypoxia, vascular (stroke, MI), space occupying lesions,
epilepsy (status epilepticus, post-ictal states), trauma/head injury,
nutritional (thiamine, nicotinic acid, B12 deficiency).
Investigations
BM stix, blood glucose, oxygen saturation (to look for hypoxia), ABGs
(hypercapnaea), Dementia screen (including FBC, U&Es, LFTs, TFTs,
vitamin B12 and folate, folate, CT, MRI, cardiology, syphilis serology),
referral to memory clinic if necessary, CXR (bronchial or lobar
consolidation), CT scan (cerebral metastasis, stroke, headinjuries),
sputum, urine and blood cultures, EEG, plasma drug levels (for antidepressants and anti-convulsants), lumbar puncture (if meningitis is
suspected).
Management
Important principles include reducing distress, and minimizing
medication. Multidisciplinary team assessment, involvement of
relevant community agencies.
Allergy and Facial Swelling

Features of a rudimentary allergy history include:
Ask about any history of weals, atopy, urticaria (well-circumscribed
erythematous weals which could also be a presenting feature of
an underlying disorder such as SLE/thyrotoxicosis/lymphoma).
Enquire about previous response to antihistamines and
prednisolone.
Find out about other symptoms (e.g. laryngeal oedema stridor,
dyspnoea), systemic disorders (fever, arthralgia, myalgia), pain
(e.g. jaw pain in neoplastic lesions of the jaw; carcinoma of the
sinuses is associated with a blocked nose and bloodstained

discharge). Puffiness around the eyelids usually indicates renal
failure.
Enquire about precipitating factors (e.g. trauma, local pressure,
emotional stress, allergen, food allergy, extreme cold, jewellery).
A full medical history should include a family history of atopy or
angioodema, and alcohol, social and occupational history.
If nephrotic syndrome is suspected, ask some focussed questions:
Ask about the circumstances of the onset of the oedema,
Elicit urinary symptoms including frequency, haematuria,
pigmentation,
Enquire about constitutional symptoms (lethargy is often associated
with renal failure).
Ask questions relating to the cause: Glomerulonephritis
(autoimmunejoint pain, rash, eye symptoms), recent bacterial
infection (streptococcal), risk fators for hepatitis B and C or episodes
of jaundice, recent foreign travel (malaria), malignancy (particularly
myeloma), diabetes (longstanding or new onset thirst, polyuria,
nocturia, weight loss), amyloid (altered bowel habit).
Also ask questions relating to complications of disease (venous
thrombosis, pneumococcal sepsis due to loss of immunoglobulins,
symptoms of renal failurelethargy, urinary symptoms). In taking
a history of nephrotic syndrome, a full previous medical history is
essential, including diabetes, malignancy, autoimmune disease.
Obtain, as usual, a drug history (e.g. penicillamine, gold, allergies),
a social history including alcohol intake, and a travel history (any
history of travel to areas of endemic malaria).
Causes of a facial swelling include:
Allergy, contact sensitivity, atopic dermatitis, cutaneous
mastocytosis and systemic mastocytosis (episodic flushing with or
without urticaria but no angioedema)
Hereditary angioedema (deficiency of C1 esterase inhibitor, with
angiooedema not urticaria)
Nephrotic syndrome
Hypoalbuminaemia
Infection: Orbital/periorbital cellulitis, dental/sinus infection
Hypo/hyperthyroidism
Dermatomyositis
Caroticocavernous fistula, cavernous sinus thrombosis
Subcutaneous emphysema
SVC Obstruction
Neoplasm (parotid, sinuses, jaw, mediastinal tumours)
Cushings syndrome, obesity
Drug-induced (steroids).
Investigations
General useful investigations include FBC (malignancy, infection), ESR,
U&Es (renal failure), skull X-rays (fractures, sinusitis, malignancy),
CXR (tumour), swab for infection. For allergy, skin prick and RAST
tests are commonly used. For nephrotic syndrome, useful investigations
include: Complement levels, 24-hour protein level, EDTA for GFR,
FBC, ESR, CRP, U&E, LFTs, glucose and HBA1c, Hepatitis B and C
serology, HIV test, serum electrophoresis and immunoglobulins,
cholesterol, ANA, dsDNA, C3, C4, ASO titre. Also: Throat swab. Urine
microscopy for red-cell castsglomerulonephritis, Other tests would
be for specific causes outlined above.
Management
If allergy, reassurance, avoid aspirin and opiates, non-sedating
histamines, laryngeal swelling will require admission to hospital for
urgent treatment and observation. If a nephrotic syndrome, the general
principles of treatment are: treat the underlying cause, dietary sodium
restriction, diuretics, prophylactic antibodies against streptococcal
infections, anticoagulation, high protein diet.
Fever of Unknown Origin

This is quite a common history station.

Useful aspects of the history include:
Pattern of fever (e.g. fever-free patterns in Pel-Ebstein fever;
intermittent (e.g. malaria), remittent fever (fever returns to normal
for a time but it is always elevated, e.g. abscess formtion,
tuberculosis and carcinoma).
Presence of drenching sweats (e.g. malignant and infective causes,
typically at 1-3 am often waking the patient up), and rigors in
abscesses.

Joint and muscles pains (e.g. connective tissue disease or vasculitis).
Skin rashes (e.g. SLE and infective endocarditis).
Ask about any changes in weight and lymphadenopathy. Relevant
respiratory, cardiovascular, gastrointesinal and neurological
symptoms (including headache and neck stiffness). Also enquire
about recent surgical history.
Obtain a full drug history. Enquire about recent travel abroad
(malaria prophylaxis and compliance: 1 week before the trip and
for 4 weeks after returning), and note especially sexual history.
Infective and malignant causes constitute 55% of cases. (1) Infective
(abscess, TB, infective endocarditis, malaria, TB, urinary tract, tropical,
EBV, CMV, Q fever, toxoplasmosis, brucellosis), (2) Cancer (lymphoma,
epithelial tumours, leukaemia, renal cell carcinoma, hepatocellular
carcinoma), (3) Connective tissue disease (SLE, polyarteritis, PMR,
rheumatoid), (4) Miscellaneous (drug, factitious, Meditteranean fever,
Crohns disease, sarcoidosis).
Investigations
Basic screening investigations are: (1) Haemoglobin, red cell indices
and blood film (e.g. anaemia, severe anaemia suggests malignancy;
iron-deficiency suggesting gastrointestinal malignancy; normochromic
and normocytic in infection, malignancy and chronic diseases), (2)
White cell count (hallmark of pyogenic infection is leucocytosis with
immature granulocytes and toxic granulation), leukaemoid reactions
(pyogenic infection, or acute leukaemia), (3) ESR (raised in most causes
of FUO), (4) Chest X-ray (abscess, pneumonia, bronchiectasis,
empyema, pulmonary infiltrates, PCP, sarcoidosis, histoplasmosis, TB
and follow-up (e.g. bronchial lavage), (5) Examination of urine (heavy
proteinuria is suggestive of renal disease, whether inflammatory or
neoplastic), (6) Cultures (sterile pyuria of TB, sputum, blood cultures,
HIV test), (7) Ultrasound/CT scan for a lesion particularly abdomen,
(8) Blood tests for connective tissue disease (e.g. antibodies to DNA,
rheumatoid factor), (9) Other: e.g. temporal artery biopsy, (10) Urinary
dipstix, (11) Tumour markers, (12) Echocardiogram, (13) White cell
scan.
Management
Loin Pain and Haematuria

Features (frequency, position, time span, radiation, nature, relieving/
exacerbating factors), associated symptoms (dysuria, haematuria,
history of prostatism), if no symptoms (IgA nephropathy, recurrent
haematuria, Henoch-Schonlein purpura with cutaneous lesions and
joint symptoms; benign familial haematuria; Alports syndrome with
bilateral sensorineural deafness), the nature of the haematuria (whether
visible throughout the stream, at the beginning of micturition clearing
towards the end of the stream or at the end of micturition), passage
of any stones, other urinary symptoms such as dysuria, poor stream,
postmicturition dribbing, past history of haematuria and prostatism,
previous history of renal stones or renal disorders (e.g. cystic disease),
history of acromegaly and activity (visual field defects, sweating,
headaches) and possible link with renal calculi, respiratory symptoms
for haematuria (e.g. cough, haemoptysis, fever, sputum), GI (changes
in bowel habit per rectum), cardiovascular (palpitations, chest pain).
Smoking and alcohol history, impact on patient. Travel history (e.g.
schistosomasis).
(1) Tumours of kidney, bladder, ureter or prostate, (2) Glomerular
pathology (IgA nephropathy, Henoch-Schonlein purpura,
glomerulonephritis, vasculitis), (3) Renal medullary disorders
(papillary necrosis due to sickle cell disease, analgesics, diabetes or
medullary sponge kidney), (4) Infection (pyelonepritis, cystitis,
prostatitis, tuberculosis, schistosomiasis), (5) Stones and trauma, (6)
Coagulation disorders, (7) Factitious.
Investigations
If there is no other renal or urinary symptom, culture urine, renal and
uterine ultrasound, consider cystoscopy; if there are deformed red
cells and/or casts and/or proteinuria, then consider renal biopsy; if
there not, renal ultrasound, and consider haemoglobin electrophoresis.
Loss of Weight
The first thing is to know how rapid the weight loss is. If rapid, this
suggests organic disease.

In the evaluaton of weight loss, the next most important factor is
loss of appetite. If the appetite is excellent with weight loss, consider
thyrotoxicosis and steatorrhoea. Two conditions commonly associated
with serious causes of weight loss are anaemia and fever, and these
must therefore be specifically excluded, including malignancy,
endocrine disease, malabsorptive states and diarrhoea.
Enquire whether clothes are looser, how much weight lost, timing
of symptoms and whether they are deteriorating, whether intentional,
current dietary intake (including cereals, ryes, wheat, barley or coeliac
disease), previous history of weight loss, previous body weight.
Important features are:
Enquire about associated gastrointestinal symptoms, e.g.
abdominal pain, nausea/vomiting, gastrointestinal bleeding
including blood in stool. There may be altered bowel habit (e.g.
suggestive of carcinoma of the large bowel). The differential
diagnosis of weight loss and diarrhoea includes: Malabsorption,
including coeliac disease, bacterial overgrowth, tropical sprue,
pancreatic disease, infective (bacterial includes Shigella and Yersinia),
protozoan (amoebic dysentery), tuberculosis, parasitic
(Strongyloides), small bowel Crohns disease causing
malabsorption, colonic neoplasm.
Enquire about specific features suggestive of an infection (e.g.
miliary TB, chronic HIV infection).
Ask about asociated endocrine symptoms (e.g. thyrotoxicosis,
tremors, increased appetite, diarrhoea, palpitations, eye symptoms;
adrenal insuffiency, weakness, dizziness, excessive sweating), drug
history (diet pills, laxatives, amphetamines).
Associated psychological factors (e.g. anorexia nervosa, anxiety
and depressive states).
Relevant medical history (gastrointestinal surgery, autoimmune
disorders including thyroid disease, IDDM, fibrosing alveolitis,
rashes), coeliac disease, gut, neoplasia, DM).
Impact of symptoms on life.
Differential diagnosis: As outlined above.
Investigations: FBC, U&Es, LFTs, iron, folate, vitamin B12, calcium,
autoantibodies for antireticulin and endomysial.
Microcytic Anaemia
A common complaint whose history can easily be messed up.

History should concern iron deficiency anaemia, thalassaemia, and
congenital sideroblastic anaemia. The majority have iron deficiency.
Causes of iron deficiency anaemia include blood loss including
menorrhagia or GI bleeding from oesophagitis, peptic ulcer,
carcinoma, colitis, diverticulitis or haemorrhoids. Poor diet may be a
cause, or malabsorption. Ask specifically about melaena or
haematemesis. In elderly women, oesophagitis due to gastrointestinal
reflux is a common cause and often asymptomatic. Bruising and
bleeding from sites such as the gums and urinary tract are serious
symptoms suggestive of thrombocytopaenia or bleeding from local
malignancy as a reason for iron deficiency. Anaemia of chronic disease
may be hypochromic).
Investigations
These include blood film, serum iron and ferritin. In iron deficiency,
there will be pencil cells, anisocytosis and poikilocytosis. Serum iron
and ferritin will be low. In anaemia of chronic disease, there is
hypochromia, and low serum iron, but there is no rise in transferrin.
If serum iron is normal, the diagnosis may be sideroblastic anaemia
or thalassaemia. Sideroblastic anaemia may be idiopathic, or occur in
anaemia, carcinoma, leukaemia or nutritional disorders. The blood
film may exhibit anisocytosis, and the bone marrow appearance with
ring sideroblasts is normal. Thalassaemia is usually demonstrated in
a blood film with target cells and basophilic cells, and diagnosis is by
haemoglobin electrophoresis which shows a moderate increase in
HbA2. Oral iron, but can cause black stools and constipation. Hb
should rise by 1g/dl/week with a modest reticulocytosis.
Continue until Hb is normal and for at least 3 months to replenish
stores.
Consider further investigation of an iron deficiency anaemia, i.e.
gastroscopy, colonoscopy, barium swallow and meal.
Management
Treat the cause.
Macrocytic Anaemia
See the initial comment for microcytic anaemia.

Useful aspects of the history of a macrocytic anaemia are:
Ask about associated symptoms, such as skin changes (e.g.
haemorrhagic manifestations and follicular hyperkeratosis of
vitamin C deficiency),
Obtain a full GI history, especially loss of weight, small bowel
disease symptoms (e.g. steatorrhea, ileal disease, bacterial
overgrowth, tropical sprue, malignancy), jaundice, sore tongue in
pernicious anaemia (glossitis), dietary history, vegan, systemic
history (heart failure, SC degeneration of spinal cord, autoimmune
disease). Obtain a past history of GI surgery (gastrectomy, ileal
resection),
Obtain a drug history (antifolate drugs, e.g. phenytoin,
methotrexate, trimethoprim).
Obtain a family history of autoimmune disorders including
pernicious anaemia, alcohol history, concern of patients.
Take a full social history including activity at home, any tiredness
or dyspnoea, poor diet or appetite.
Causes: (1) Lack of vitamin B12, due to dietary intake poor (strict
vegetarians, fish tapework), lack of intrinsic factor (pernicious anaemia,
total gastrectomy, partial gastrectomy), due to failure of intestinal
absorption (disease or resection of terminal ileum; stagnant loop
syndrome; tropical sprue) or (2) Lack of folic acid (due to inadequate
intake, e.g. dietary deficiency, pregnancy, chronic haemolytic anaemia,
or lack of absorption, e.g. coeliac disease, tropical sprue,
anticonvulsant drugs).
Investigations
Vitamin B12 and folate levels, LFTs bilirubin, parietal cell antibodies,
bone marrow examination, Schilling test if serum B12 is low with and
without intrinsic factor to be confirmed with antiintrinsic factor and
antiparietal cell antibodies. If a patient is found to be folic acid
deficient, investigation of any steatorrhoea will be needed.
Management
Treat vitamin B12 deficiency with hydroxocobalamin (please note that
this is parenteral treatment (IM) to total of 5 mg over 3 weeks then 1
mg im every 3 months for life). Folate replacement, if folate deficient.
Pain
Pain may be a feature of any history referred by a GP, and it is important
not to approach this symptom in a haphazard fashion.

Consider the characteristics of the pain character (quality of pain
for example, neuropathic pain feels burning, stabbing or shooting,
and bone pain may be described as aching or throbbing, and variation
of the pain), location, duration and alleviating factors, any decreased
mobility, sensory symptoms.
A full social history is essential: Where does he live and with whom?
Severe pain may disrupt sleep and cause insomnia, anxiety and
depression. Ask about stairs/stairlift at home, any help at home, any
help with shopping, washing and cooking. Ask also the patient whether
he/she is able to leave house or not. Obtain the patients perception
of the pain (misconceptions can lead to the patients suffering; the
patients insight and understanding can be ascertained).
Management
Treat the underlying cause (e.g. antibiotics for cellulitis, surgical
fixation for a pathological fracture).
In pharmacological treatment, the principles of a pain ladder of
analgesic use are used. Prescribe regularly, and use the oral route for
the majority of patients. One starts with simple analgesia (NSAIDs,
paracetamol), moving onto weak opiods (codeine, dihydrocodeine,
tramadol) compound preparations (co-dydramol), eventually moving
onto opiates (e.g. morphine, diamorphine) but laxatives and
antiemetics may be needed. Morphine should initially be given every
4 hours to titrate the dose, the starting dose being 2.55 mg; once a
stable dose has been achieved it is switched to a 12-hour, slow-release
preparation of morphine sulphate. The route should be oral, unless
the patient cannot take drugs by mouth. Patients in pain do not become
addicted and morphine does not also result in clinically significant
respiratory depression; the dose may need to be increased with time
due to tolerance. Monitor frequently.
Also consider non-pharmacological methods for pain and
multidisciplinary input may be useful (e.g. TENS, local blocks,
relaxation techniques, cognitive behavioural therapies).
Painful Shins
This is seen often by GPs, and therefore could easily be referred on.
Therefore, examiners would expect you to deal with this in a
reasonable methodological fashion.

Site, shape, size, colour, raised/flat, painful/painless, systemic
symptoms, symptoms suggestive of sarcoidosis, recent infection
especially. TB, myocoplasma, Yersininia, campylobacter, Salmonella,
tuberculosis, streptococcus, drug history especially OCP, penicillin,
sulphonamides, other inflammatory conditions (including thyroid
disease and inflammatory bowel disease) travel abroad, impact on
life.
Diagnosis
Erythema nodosum (females, arthralgia, fever, malaise, blue-red
nodules, lower limbs and shins).
Causes
Sarcoidosis, infection (Bacterial: Streptococcus, Chlamydia, TB,
Yersinia, Rickettsia, leprosy, leptospirosis; Viral: EBV; Fungal:
Histoplasmosis, coccidiomycosis, histiomycosis; Protozoal:
Toxoplasmosis), drugs (e.g. sulphonamides, penicillins, OCP,
salicylates, dapsone), pregnancy, malignancy (lymphoma and
leukaemia), inflammatory disorders (inflammatory bowel disease),
sarcoidosis, Behcets disease.
Investigations
CXR, ESRs, sputum, bacteriology (anti-streptolysin O titre, sputum
or early morning urine), Mantoux test, serum ACE.
Management
Treat with bedrest and NSAIDs, oral steroids, stop OCP.
Pruritus
A common complaint, and you should be guided initially by the GP
referral letter. The author is aware of one history in the real
examination where the examiners were looking for dermatitis

herpetiformis in the context of coeliac disease, in a lady who had
been unable to adhere to a gluten-free diet, but the patient wished to
know why her children were itching too, but as it happens the locum
GP had previously already diagnosed the condition as as scabies.

Timing, parts of body affected, relieving actors or provoking factors
(bath oils, stress, depression, drugs, foods, hot baths as in
polycythaemia), effects on sleep and work, whether localised or not
(e.g. scabies infection, urticaria, dermatitis herpetiformis, pruritus
vulvae and pruritus anae), associated skin rashes, living conditions
and contact history (e.g. scabies), occupational exposure (e.g. fibreglass).
Ask about associated features (haemoptysis, chronic cough and
weight loss may be suggestive of a bronchial carcinoma; night sweats
and weight loss may suggest Hodgkins disease).
Ask about the usual features of thyroid disease and renal failure
(e.g. lethargy, anorexia, oliguria, polyuria, haematuria, proteinuria,
skin fragility, oedema and bone pains).
Enquire about psychiatric features, and systemic symptoms (e.g.
tiredness, jaundice for PBC and haemochromatosis), fever, weight
loss (malignancy, lymphoma), features of thyroid disease, chronic renal
failure, history of HIV, Enquire also about drugs including herbal
remedies and recreational/domestic agents, e.g. biological washing
powders, alcohol and smoking history.
Ask about the impact of symptoms of the pruritus on life.
(1) Obstructive liver disease, (2) Haematological disorders (irondeficiency anaemia, polycythaemia; consider whether the pruritus is
worse after a hot bath or shower), (3) Endocrine (hyperthyroidism,
hypothyroidism, diabetes mellitus), (4) Chronic renal failure through
calcium-phosphate product, (5) Malignancy (internal malignancy and
lymphoma), (6) Drugs (e.g. morphine), (7) Others, e.g. pregnancy and
senility, (8) Malabsorption: In steatorrhoea (especially with that of
gluten-sensitivity), (9) Collagen disorders (e.g. scleroderma).
Management
Treat underlying cause, e.g. cholestyramine and ursodeoxycholic acid
for PBC.
Purpuric Rash
Ask about the concerns of the patient. Useful factors to consider for
purpura are:
How long have the symptoms been present for (e.g. early in life,
adolescence, adulthood)?
Distribution of the rash.
Description (size, shape, circumscribed, itchy, blanching).
Ask about any enciting cause (e.g. dental extraction, cut, site, mucosa
or joint).
Ask about operations and tooth extractions, and past attacks of
joint swelling. Haemophiliacs usually notice their symptoms when
they run around and hurt themselves. Ascertain the extent of the
bleeding.
Ask about haemarthrosis, a feature of many bleeding disorders,
e.g. haemophilia A and B, and polyarthritis may accompany
diseases in which bleeding is a feature, e.g. purpura, SLE, and
drug sensitivity.
Associated symptoms (malaise, febrile symptoms common in
leukaemia and acute thrombocytopaenia, epistaxis, weight loss
(leukaemia, secondary malignancy)).
Ask about other haematological symptoms that might suggest bone
marrow disease: Platelet disease (e.g. melaena, haematuria,
haemoptysis), red cell disease (ankle swelling, breathlessness),
white cell disease (increased susceptibility to infection).
Relevant past medical history of lymphadenopathy, liver disease
or viral infections, bleeding/coagulopathies.
A full drug history (includes anticoagulants, steroids,
sulphonamides, chloramphenicol, non-prescription drugs, gold,
carbamazepine, substance abuse).
Dietary history (vitamin C deficiency).
Family history of haematological disease or organ-specific
autoimmune disease.
Systems review (abdominal pain, malabsorption, arthralgia,
pruritus).
Bone failure (e.g. leukaemia, infiltration by secondary malignancy),
coagulation deficiency (TTP, DIC, HUS), drug-induced (e.g.

sulphonamides, chloramphenicol, steroids), infection (e.g. EBV, CMV
and toxoplasmosis) and others such as Henoch-Schonlein purpura.
Investigations
Full blood count for thrombocytopaenia, liver function tests, and blood
film (if leukoerythroblastic, this is suggestive of marrow infiltration,
causes of which include carcinoma, lymphoma or myelofibrosis).
Consider causes of thrombocytopaenia: (1) Bone marrow infiltration
includes acute leukaemias, CLL and CML, (2) Bone marrow depression
(e.g. drug, toxic, uraemic), (3) Increased platelet destruction (ITP),
(4) Intrinsic platelet defects (e.g. myeloprolifertive disorders). Other
causes to consider: (1) Cryoglobulinaemia and paraproteinaemias, (2)
Vitamin K and specific factor deficiencies, (3) DIC. The most important
next investigation is bone marrow aspiration or trephine. Other
investigations include blood urea, radiological skeletal survey, protein
electrophoresis or ANF.
Management of ITP
(Women, 20-40, abrupt fall in platelet count, thromboytopaenia, platelet
antibodies, consider EBV serology for splenomegaly). Treatment with
IVIG. Emergency splenectomy for desperately ill.
Tiredness
Points in History
Whatever the aetiology of the tiredness, it is useful to ask a few
detailed questions.
What does the patient actually mean by tiredness?
Are the symptoms episodic?
Do they occur at specific times of the day (for example, rheumatoid
arthritis causes morning stiffness which improves with activity).
What is the duration of lethargy?
What is the effect on routine activities (in particular, how the
tiredness affects work and home wife, and whether or not there
are any factors the patient can identify which contribute to the
way he/she feels).
Ask about social factors (e.g. sleep deprivation which may be selfinduced, noisy neighbours, new work and domestic pressures,
new child).

Past history of neoplasm, viral illness, thyroid disorder or surgery,
diabetes mellitus or psychiatric illness, psychological symptoms
(stress/anxiety/depression), occupational and smoking history,
drugs including anxiolytics and benzodiazepines, concerns of
patient. Investigation and management according to cause.
Enquire about symptoms which might suggest important causes:

Haematological, e.g. anaemia, pallor, per rectal or vaginal bleeding;
Endocrine, e.g. hypothyroidismpreference for warmth, weight
gain, dry skin, hair thinning) Addisons disease (postural dizziness),
Respiratory, e.g. obstructive sleep apnoea (snoring), chronic lung
disease, lung cancer (cough, haemoptysis).
Cardiovascular heart failure (dyspnoea),
Gastrointestinal inflammatory bowel disease (changing bowel
habit), colorectal cancer (changing bowel habit),
Infection, (e.g. infectious mononucleosis lasting a few weeks,
tuberculosis, Lyme disease),
Neurological, (e.g. myaesthenia gravis, proximal myopathy
specifically causing muscle fatigue).
Psychiatric depression (sleep disturbance, change in appetite or
weight), chronic fatigue syndrome (fatigue after minimal activity,
associated with aching muscles).
Others, iatrogenic (-blockers), renal failure, limb weakness
(including the very rare cause of periodic paralysis).
Say that you would also try to obtain a history from a relative.
Investigation
As above, including a chest X-ray, FBC, ESR, monospot, liver function
tests, thyroid function tests, calcium.
Management
Cardiovascular
System (Station 3)

INSPECTION
General inspection is specifically stated on the marksheet, and this is
because of its relevance to the overall cardiological examination.
Look for signs, whilst introducing yourself/repositioning, of certain
systemic disorders:
Acromegaly: Spade-like hands, widely-spaced teeth, protruding
tongue, coarse facies.
Marfans syndrome: Tall-thin habitus, spindle fingers
(arachnodactyly), wide arm span, high-arched palate.
Ankylosing spondylitis: Question-mark posture, aortic incompetence
seen in approx 1% of patients.
Specific
Breathlessness High respiratory rate,
Failure to maintain semi-recumbent position,
Identify finger clubbing (loss of nail bed angle, increased transverse
curvature, drumstick appearance increased angle between nail plate
and posterior nail fold; causes, cyanotic congenital heart disease,
infective endocarditis), cyanosis (right to left cardiac shunts) and
stigmata of endocarditis (Oslers nodes, Janeway lesions, splinter
haemorrhages, digital infarcts).
Look for abnormalities of complexion: Anaemia pallor/
koilonychias (causing heart failure, tachycardia), polycythaemia. Malar
flush signs of pulmonary hypertension, seen with mitral stenosis
and primary pulmonary hypertension.
A visible earlobe crease is stastically correlated with coronary
artery disease, especially in the Asian population.

Clicks listen carefully for the audible clicks of a clean prosthetic
heart valve. Dont be fooled into thinking that the audibility implies
it is a metallic valve, as biological valves may also produce audible
clicks. Complex metallic valves may have more than one metallic sound,
making identification of the replaced valve difficult. Similarly,
concomitant AF makes timing with diastole-systole difficult. Systolic
murmurs are often heard and do not suggest dysfunction but diastolic
murmurs always indicate malfunction.
Jugular Venous Pressure

The candidate is expected to inspect the JVP. The right internal jugular
vein should be used in preference to the left. The JVP is the vertical
height of the pulse above the sternal angle. With the patient semiprone, assess the character of the waveform (canon a wave, CV waves
seen in time with the arterial pulse hence the alternative term systolic),
X and Y descents of pericardial tamponade; frequently the earlobe
may be seen to oscillate, with tricuspid incompetence (very prominent
CV waves). Time A (atrial contraction) and V wave (tricuspid
valve drawing away from the right atrium; synchronous with the
carotid pulse).
Specific patterns of jugular venous pressure in relation to certain
valvular abnormalities:
Tricuspid incompetence X descent is lost and replaced by very
prominent right systolic waves, synchronous with the carotid pulse
called systolic V waves.
Pulmonary stenosis, pulmonary hypertension, tricuspid stenosis
large a waves.
Constrictive Pericarditis
Paradoxical rise in the JVP on inspiration (Kussmauls sign), prominent
X descent and sharp Y descent.
Complete Heart Block

Giant A or cannon waves when the atrium contracts on a closed
ventricle. They are therefore found in patients with ventricular
pacemakers and in patients with complete heart block or ventricular
extrasystoles.
Atrial flutter A wave is lost because effective atrial contraction is
lost.
Cardiovascular System (Station 3) 121
Chest Wall
Chest wall shapes: See Station 1: Respiratory system.
Operation scars: Median sternotomy (CABG or prosthetic heart valve
replacement; check vein graft sites), left lateral/inframammary
thoracotomy (closed mitral valvotomy) may be missed under the left
breast unless specifically sought for, pacemaker/AICD implant
(infraclavicular scar with the device often palpable): Note that
pacemakers are usually inserted on the non-dominant side
(handedness-wise) for convenience of the patient. Never mistake a
mastectomy scar for an inframammary scar. Dont miss the scars of
an AV fistula in the ante-cubital fossa.
Oedema: Look down to ankles, expose if covered. Check for pitting;
depress for 3 seconds and release finger. When examining posterior
lung fields, check for the presence of sacral oedema.
PALPATION
Pulse
The candidate is expected to check the pulse, and derive as much
information as possible.
At the radial artery, determine the rate (count for 15 seconds),
rhythm (sinus, irregular), character (weak/bounding). Ideally, the
carotid artery should be palpated to determine the character of the
pulse. Different types of pulse that should be recognised are stated
clearly in the MRCP Clinical Guidelines.
Characteristics of the Pulse

Slow rising pulse: Or plateau or anacrotic pulse, delayed percussion
wave, palpable judder on the upstroke, narrow pulse pressure.
Sharp upstroke jerky pulse: May be a sign of hypertrophic
cardiomyopathy, ventricular ejection stops and starts. Pulse may
be jerky if a large volume of blood regurgitates into the left ventricle
with reduced systolic ejection time.
Small volume collapsing pulse: Associated with ventricular run-off
states such as mitral regurgitation or ventricular septal defect. There
is a quickly rising small percussion wave.
Collapsing pulse: To examine for a collapsing pulse, place the three
middle fingers across the strongest brachial impulse and then
slowly lift up the arm, after establishing whether the patient has
any shoulder discomfort, above the level of the heart.

Simultaneously feel the other radial pulse to note any radio-radial
delay (pre-subclavian coarctation, cervical rib). Brisk upstroke with
collapse following, occurs in av fistula, aortic regurgitation, patent
ductus arteriosus; if large volume, consider thyrotoxicosis, Pagets
disease, severe anaemia.
Low volume: Aortic stenosis.
Pulsus alternans: Alternating large and small beats, sign of left
ventricular failure, common in aortic stenosis.
Paradoxical pulse: Excessive fall in pulse pressure > 10 mm Hg during
inspiration, which may occur physiologically, cardiac tamponade,
peripheral constriction, acute severe asthma.
Sinus bradycardia: Causes: Fitness, ageing, MI, drugs,
hypothyroidism, obstructive jaundice, raised intracranial pressure,
hypothermia, hyperkalaemia. Temporary/Permanent Pacing if
symptomatic 2nd or 3rd degree heart block, complete heart block,
symptomatic bradycardia.
Sinus tachycardia: Causes: Fever, anaemia, heart failure,
thyrotoxicosis, phaeochromocytoma, carcinoid syndrome, drugs
such as nifedipine and theophylline.
Atrial flutter- fibrillation: Look for malar flush, mitral valvotomy,
elevated JVP without a waves. Differential: AF, multiple ventricular
ectopics, AF with variable block, complete heart block. Causes:
Mitral valve disease, IHD, thyrotoxicosis, constrictive pericarditis,
chronic pulmonary disease, hypertensive heart disease,
cardiomyopathy, acute infections (particularly lung), local
neoplastic infiltration (particularly lymphoma).
Radio-femoral delay: Coarctation of the aorta.
Absent radial pulse: Absent radial artery, abnormal position of the
radial artery, catheterization of the brachial artery with poor
technique, subclavian artery stenosis, Blalock-Taussig shunt, A-V
shunt for dialysis, embolism into the radial artery, Takayasus
arteritis.
Apex Beat
Move swiftly to the precordial region and localise the apex beat by
starting out in the axilla and then moving medially (showing the
examiner that you are considering left ventricular enlargement). Be
seen to be counting down the rib spaces with the other hand, keeping
the localising hand still. A displaced apex beat has a number of
important causes: Volume overload, aortic regurgitation, mitral

regurgitation. Determine the character of the apex beat as this may
help determining the dominant pathology in patients with mixed
valvular disease. Additionally, by placing the flat of the hand over
the line of the lower heart border and by placing the hand over the
precordium (left parasternal area), you may be able to detect any
palpable heaves.
The candidate should be able to distinguish different types of apex
beat:
Double impulse: May be a sign of hypertrophic cardiomyopathy.
Tapping apex: Palpable equivalent of loud S1 (mitral stenosis).
Hyperdynamic/Thrusting apex: Aortic incompetence.
Sustained apex: Aortic stenosis.
Heaving apex: Left ventricular hypertrophy.
Impulses
The candidate should test for and recognize abnormal cardiac impulses
such as:
Right ventricular parasternal lift/right ventricular heave/left
parasternal heave: Usually a consequence of pulmonary
hypertension.
Left ventricular dyskinesia.
Palpable heart sounds: Thrill at apex, consider mitral regurgitation;
upper parasternal thrill, consider aortic stenosis (right parasternal
edge) or pulmonary hypertension (left parasternal edge).
Measurement of Blood Pressure

The candidate should be famililar with the technique of measurement
of arterial blood pressure with a conventional syphgmomanometer
using standard or large cuffs. Phase V recordings are acceptable as
diastolic blood pressure.
Percussion
Percussion of the cardiac border or area of dullness adds little to the
clinical assessment in modern practice.
Auscultation
Candidates should remember that the examiners will have agreed
the signs that they are expected to elicit, using standards appropriate
for the level of competence required.
CHARACTERISTICS OF HEART SOUNDS

Loud S1: Tachycardia, hyperdynamic circulation, short PR interval,
mitral stenosis with mobile valve.
Wide expiratory splitting: When right ventricular emptying is slow
(pulmonary stensosis/RBBB) or left ventricular emptying is fast (mitral
regurgitation).
Reverse splitting: When right ventricular emptying is fast (right
ventricular pacing) or left ventricular emptying is delayed (e.g. LBBB,
aortic stenosis, HOCM).
Fixed splitting: Wide fixed splitting in ASDs.
Loud S2: Tachycardia, systemic hypertension (loud A2), pulmonary
hypertension (loud P2).
Ejection click: Aortic stenosis or pulmonary stenosis.
Opening snap: Mitral stenosis (high pitched sound caused by high left
atrial pressure snapping open the valve).
S3: Rapid left ventricular filling in early diastole, hyperdynamic states,
heart failure and mitral regurgitation.
S4: Vigorous atrial contraction on a stiff ventricle, systemic
hypertension, aortic stenosis, left ventricular hypertrophyalways
pathological.
Mid systolic click: Mitral valve prolapse.
Metallic prosthetic sounds (see below).
Auscultation Technique
The candidate should be familiar with the surface markings of the
four valve areas and be able to time murmurs to diastole and systole
(e.g. mid, late or pansystolic) or continuous. The loudness/intensity
of the murmur should be described. The candidate may use a grading
system. If appropriate, auscultation should be performed with the
patient in different positions. A murmur is heard, the candidate should
also auscultate the carotid arteries, lateral chest, and the posterior
chest to assess the radiation of the murmur and basal crepitations
(for left ventricular failure). The candidate should also be able to
differentiate between innocent murmurs and murmurs related to
significant valvular lesions.

Complete the examination by offering the blood pressure, peripheral
pulses, sacral or peripheral oedema, assessment of the lower limb
pulses, urinalysis and fundoscopy for signs of hypertension.
ENDOCARDITIS PROPHYLAXIS
This is subject to change but please check with the British National
Formulary at time of publication.
Common Cases
of a diagnosis or differential diagnoses. Common cardiology cases
IRREGULAR PULSE/ATRIAL FIBRILLATION

This man feels fine and has been referred by his GP due to an
abnormality found on his cardiovascular examination. Please examine
that system and report any abnormal findings.
Pulse is chaotic both in rhythm and volume irregularly irrregular.
Radial pulse is less than apical pulse deficit.
JVP No a wave.
Apex Normal unless other disease, e.g. mitral senosis.
Auscultation S1 varies in intensity and S2 is normal.
Consider the aetiology, e.g. features of mitral valve disease or
thyrotoxicosis.
Symptoms: Usually none, paroxysmal palpitations, fatigue and
dyspnoea, presyncope and dizziness, embolic symptoms clinical
features of mitral stenosis, symptoms of the underlying cause.
Aetiology: Ischaemic heart disease, mitral valve disease, hyperthyroidism, hypertension, pulmonary embolism, cardiomyopathies, alcohol,
constrictive pericarditis, sick-sinus syndrome, lung pathology, e.g.
carcinoma, pneumonia.
Differential diagnosis: Ectopic beatsatrial or ventricular. Unifocal
ectopics have a constant compensatory pause after the beat. Dropped
beats are followed by a normal RR interval. Multifocal ectopics can
result in a truly chaotic pulse. Wenckenbach AV block has a
progressively lengthening RR interval, followed by a dropped beat.

Sinus Arrhythmia
Investigations: Treat the underlying cause. Is this paroxysmal, persistent
or established AF? Does the patient warrant anti-coagulation? In
paroxysmal or persistent AF, the aim is cardioversion, and then
maintenance of, sinus rhythm; if this is unattainable, aim to minimise
the duration and frequency of AF. Atrial systole may contribute up
to 25% of cardiac output by increasing the LVEDV, and may be
symptomatically critical in patients with poor LV function.
Cardioversion is either chemical or electrical. Warfarin is the
anticoagulant of choice, to give the INR between 2.0 and 3.0. In
patients, where rate control is preferable to conversion to sinus rhythm,
digoxin, -blockers and calcium channel antagonists are all effective.
Urgent DC cardioversion is the treatment of choice in the
haemodynamically compromised patient. In those patients with AF
of less than 48 hours, cardioversion can be generally undertaken
without the need for prior anticoagulation with warfarin, although
hepatin cover is advisable. Transoesophageal echocardiogram is often
employed to exclude intracardiac thrombus.
METALLIC PROSTHETIC VALVE REPLACEMENT

This patient has recently been treated for shortness of breath. Please
examine his cardiovascular system, and discuss what precautions (if
any) are needed for an upcoming routine dental extraction.
An Extremely Common Cause

Clinical symptoms: Prosthetic valve endocarditis (any unexplained
malaise, fever, weight loss, dyspnoea; any dental treatment in the
last 6 months with no antibiotics; change in valve sounds; new
symptoms); systemic embolization (commonest with mechanical
valves, approximately 1% per year even with ideal anticoagulation);
dyspnoea associated with a failing valve this is a predictable feature
of biological valves which fail more rapidly than mechanical valves;
haemolysis, valve thrombosis, valve dehiscence, myocardial failure
and arrhythmias may occur.
Clinical signs: Audible prosthetic clicks (metal) on approach and scars
on inspection. The closing sound is the dominant one with both valves.
Disc valves tend to produce a clicking noise on opening or closing
while ball and cage valves have a characteristic plopping sound.

Aortic valve prosthesis: 1st heart sound normal, ejection click, ejection
systolic murmur, click at the second heart sound.
Mitral valve prosthesis: Click at 1st heart sound, opening click in diastole.
A regurgitant murmur should be regarded as pathological and
indivative of valve failure.
Note that tricuspid valve prostheses tend to be bioprosthetic, as
the risk of clot due to the nature of flow on the right-side of the heart
is slower.
Extra points: Bacterial endocarditis signs, valve failure, stigmata of
anti-coagulation (bruises, metal valve) or embolic disease, anaemia.
Inspect the teeth meticulous dental care is vital.
The opening and closing sounds of either ball or disc should be
clear and sharp and not muffled. Vegetations may muffle the sounds
or restrict movement.
Cause: Multiple valve murmurs/replacements; rheumatic fever;
saphenous vein harvest scars: aortic valve replacement more likely.
Choice of Valve Replacement

An advantage of a metallic valve is that it is comparatively durable.
However, warfarin is needed. Metallic valves are indicated for young
patients, Porcine valves, in contrast, do not require warfarinisation
of the patient, but they are less durable. They are most suitable for
elderly people or those at risk of haemorrhage. Note however, that
the choice of the valve is ultimately the patients choice. Even young
women who wish to become pregnant may have a metallic valve
inserted because of the option of low-molecular weight heparin as
the mode of anti-coagulation. Currently the operative mortality is
around 3-5%, with survival @ 10 years, 50%.
Late complications: Thromboembolus 1-2% per annum despite warfarin,
bleeding 1% per annum on warfarin, prosthetic dysfunction and LVF;
haemolysis (mechanical destruction against the metal valve); valve
regurgitation; infective endocarditis.
Types: Ball-and-cage ball devices (e.g. Starr-Edwards), pivotal single
tilting disc (e.g. Bjork-Shiley) and double leaflet valves: All require
anti-coagulation for life. More durable, but greater risk of
thromboembolism than xenografts. The partner can be disturbed by
the audible clicks.

Midline sternotomy scar, metallic S1/S2.
Complex metallic valves may have more than one metallic sound,
making identification of the replaced valve difficult.
Biological valves: Homografts (cadaveric) and xenografts (porcine or
pericardium mounted on a frame). Most prosthetic mitral valves are
inserted in patients with AF, who thus require anticoagulation.
Xenografts are less durable and need replacing in 8-10 years; they are
less durable in younger patients, but better in the elderly. Homografts
are the first choice in a young patient needing an aortic valve, but
they may degrade with time. Historically, women of childbearing
age received bioprostheses due to theoretical concerns of fetal
abnormalities with warfarin.
Features of decompensation: Thromboembolic sequelae, infective
endocarditis, leakage, dehiscence, ball embolus, valve obstruction due
to thrombosis and clogging, haemolysis with anaemia, fracture, poppet
escape, calcification. Mechanical valves are increasingly preferred to
biosynthetic valves because of lower re-operative rates. Endocarditis
risk is higher. Bioprosthetic valves may be more suitable for patients
where anticoagulation is a risk/patients unlikely to live longer than
the prosthesis, patients over 70 requiring AVR as the rate of
degeneration is slow.
Investigations: CXR, refer endocarditis to a prosthetic valve to a
cardiothoracic centre, endocarditis (cultures, ESR, CRP, FBC, echo,
24-hr tape for transient arrhythmia).
Management: The guidelines on oral anticoagulation (3rd edition, 1998)
state 3.5 as the target INR for mechanical prosthetic valves (not
indicagted for bioprosthetic valves where aspirin can be used for the
first few months). An effective relatively low intensity regimen (INR
3.0 4.0) is supported by the latest analysis of a large Dutch study
equating actual INRs to events (Cannegieter et al. 1995). Different
valves have different targets, according to some clinic (e.g. bileaflet
valves need an INR of 2.0 3.0), whereas, Starr-Edwards valves need
an INR of 2.5 3.5.
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY AND

PACEMAKER
This young man has complained of palpitations whilst playing football.
Examine his cardiovascular system.
Caused by mutations in contractile proteins.
Symptoms
Often asymptomatic;
Chest pain (around 50%);
Palpitations (associated with WPW syndrome);
Syncope (15-25%) or sudden unexpected death; dizziness;
Angina can occur even with normal coronary arteries;
Dyspnoea on exertion can be due to a stiff entricle in diastole,
thus reducing atrial transport.
Exercise often exacerbates these symptoms and may induce
syncope.
Signs: Prominent pressure-loaded double apical impulse and
pansystolic murmur at the apex due to mitral regurgitation, and
ejection systolic murmur at the left sternal border starting well after
S1 towards the axilla (across the outflow tract obstruction), accentuated
by squatting. Pulse jerky in character with large tidal wave. The
murmur is accentuated by forceful expiration or the Valsalva
manoeuvre (raising the intrathoracic pressure), and is diminished by
deep inspiration or the Muller manoeuvre. Atrial impulse can often
be felt the double apex. Systolic thrill present at the lower left
sternal edge.
Differential diagnosis: Aortic stenosis, subvalvar mitral regurgitation,
VSD. Up to 70% of cases are inherited as an autosomal dominant
condition, with a variable degree of penetrance and equal sex
distribution. There is a large degree of genetic heterogeneity which
accounts for the wide spectrum of HCM. Mutations on the gene coding
for Troponin T at 1q3 carry the worst prognosis. The identification of
the gene in an individual of the gene in an individual or family may
enable an earlier and more precise diagnosis, and enable more useful
prognostic information to be given.
Associations: Associated mitral valve prolapse (MVP), family history
of Fredreichs ataxia or myotonic dystrophy, family history.
Investigations: ECG: LAD, LVH, large Q waves (V1-V3) and inverted
T waves (V1-V3). Normal in 25%. ST-T and T-wave changes and tall
QRS in mid-precordial leads, WPW syndrome, ventricular ectopics.
Q wave in inferior and lateral precordial leads. Exercise ECG, 24hr
ECG (ventricular tachycardia). CXR: Normal unless heart failure.
Echocardiogram is diagnostic and to assess left ventricular structure
and function, valvular regurgitation and atrial dimensions.

Characteristic finding is of systolic anterior motion of the mitral valve
(SAM) on M-mode. Mid-systolic aortic valve closure. Cardiac catheter
echocardiography has reduced the need to pass a catheter into the
excitable and unstable LV, which often induces VT. But it does
document the withdrawal gradient, any MR and blood flow in the
coronary arteries; it is also used for electrophysiological studies in
the WPW syndrome.
Treatment: Nitrates should be avoided for angina as they increase the
outflow obstruction; -blockers are the mainstay of treatment for
giddiness, syncope, angina and dyspnoea; amiodarone is given for
SVT; infective endocarditis may occur. Genetic testing, but the
genotype-phenotype correlation is uncertain. Dual-chamber pacing
with depolarisation from the RV apex alters septal motion and is a
promising alternative to surgery. Dual-chamber pacing is required as
atrial transport is so important in HCM. Surgical myotomy or
myomectomy through the aortic valve effectively reduces the left
ventricular outflow tract gradient more than pacing but with a higher
mortality risk. Implantable cardioverter defibrillators should be
considered in those at risk of sudden cardiac death.
PERICARDITIS AND PERICARDIAL EFFUSION

This man is short of breath. Please examine his cardiovascular system
and suggest why.
Features of a constricted perdicardium: Pericardial rub, raised JVP,
prominent X and Y descents, non-pulsatile heapatomegaly.
Causes: Viruses, TB, SLE, malignancy, Dresslers, renal failure. Look
for signs of SLE and other immune disease and weight loss (for TB or
malignancy).
Pericarditis may lead to pericardial effusion and even tamponade
(small volume pulse, hypotension, raised JVP). ECG shows small
complexes.
Echocardiogram: Volume of fluid, cardiac contractility, guide
pericardiocentesis.
AORTIC STENOSIS
and suggest why.
Aetiology: Either valvar, subvalvar or supravalvar.

Valvar stenosis is the commonest (congenital in 7% M:F 4:1,
bicuspid aortic valves are present in 1% of the population); it is the
commonest cause of AS in the 40-60 year age group. Inflammatory
rheumatic fever causing AS and AR. Arteriosclerosis in type Ia
hypercholesterolaemia; gross atheroma can involve the aortic wall,
the major arteries, coronary arteries and aortic valve.
Subvalvar: Discrete fibromuscular ring, HCM.
Supravalvar: A constricting ring of fibrous tissue at the upper
margin of the sinus of Valsalvaassociated with Williams syndrome
(hypercalcaemia, giant a wave in JVP, PA stenosis RVH, P thrill,
elfin facies, mental retardation) due to mutations in the elastin gene.
Associations: Coarctation, angiodysplasia.
Symptoms: Left ventricular hypertrophy occurs with a compensatory
enlargement of the coronary circulation. There is a relatively fixed
cardiac output, and thus the heart is at its maximum output at rest.
Angina: The increased muscle mass and increased pressure in the
heart muscle, in both systole and diastole, increase oxygen demand
while decreasing supply.
Dyspnoea: The increased pressure within the LV increases further
with exercise.
Paroxysmal nocturnal dyspnoea and orthopnoea supervene as the
LV function deteriorates.
Giddiness and syncope: On exertion, the relatively fixed cardiac output
cannot increase further.
Sudden death can occur.
Emboli: Can arise from the calcified valve.
Symptoms of infective endocarditis can be seen.
Features: Pulse is regular, low volume with delayed upstroke (judder),
slow rising pulse, narrow pulse pressure, undisplaced heaving apex
beat, systolic thrill over apex area; S4; S3. harsh ejection systolic
(crescendo-decresendo) murmur radiating to neck. The carotids may
be difficult to palpate in severe disease.
Venous pressure is not elevated.
Systolic blood pressure is low normal.
Signs of severe aortic stenosis: Pulsus alternans, narrow pulse pressure,
slow rising pulse, soft S2, reversed S2, aortic systolic thrill/heave in
the second right intercostals space, left ventricular failure, S4, cardiac
failure, dispalced apex (Note, in real life, the pulse pressure can be
wide in view of the rigid peripheral circulation).

Echocardiogram: The definition of aortic stenosis is based on the valvular
area, the normal area being around 3 cm2. Aortic stenosis is normally
graded as mild, moderate or severe. Mild valve area > 1.5 cm 2,
moderate valve area > 1.0 to 1.5 cm2, severe valve area < 1.0 cm2,
critical area < 0.75 cm2.
Progression is manifest as a reduction in valve area and an increase
in transvalvular systolic pressure gradient. Some factors of significance
in rapid progression are aortic jet velocity, degree of valvular
calcification, hypercholesterolaemia, renal impairment,
hypercalcaemia.
Differential diagnosis: HOCM, VSD, aortic sclerosis (normal pulse
character and no radiation of the murmur), aortic flow murmur,
innocent flow murmur (pregnancy, fever, anaemia, thyrotoxicosis),
ASD, VSD.
Investigations: ECG (usually shows LVH found in 85% of patients
with significant aortic stenosis and possibly left axis deviation, STT changes, LBBB or CHB), CXR (cardiac enlargement and poststenotic
aortic dilatation, pulmonary oedema and LVF), echocardiogram
(bicuspid valve, calcifiation, LVH and function, AR, gradient
assessment), not exercise testing. Cardiac catheter to confirm and
clarify diagnosis, gradient, LV function, aortic root size, and assess
coronary circulation prior to surgery.
Complications: (a) Endocarditis (splinters, Oslers node, Janeway
lesions, Roth spots, temperature, splenomegaly, haematuria, petechial
rashes on the skin and conjunctivae, conjunctivae for anaemia, immune
complex phenomena manifest through glomerulnephritis or
neuropsychiatric complications), (b) Left ventricular dysfunction:
Dyspnoea, displaced apex, bibasal crackles, (c) Conduction problems
Acute (endocarditis) or chronic (calcified valve); ventricular
arrythmias are more common than supraventricular arrhythmias, and
heart block may occur because of calcification of conducting tissues,
(d) Sudden death.
In the late stages of aortic stenosis, when cardiac failure and low
cardiac output supervenes, the murmur may become markedly
diminished in intensity.
Treatment: Symptoms (syncope, chest pain or dyspnoea), asymptomatic
with mean gradient > 50 mmHg. This figure is only a guide and
operation may be indicated with a lower gradient if the cardiac output
is low. Valve replacement is required as valvuloplasty offers limited

benefit in adults. Age alone is not a contraindication. Asymptomatic:
Regular review 6/12, antibiotic prophylaxis for dental, genitourinary
and colonic investigations or treatments. Nitrates and ACE inhibitors
should be avoided as they increase the gradient across the valve
(reduce afterload). Critical coronary lesions should be bypassed at
the same time. The average survival (without surgery) once symptoms
of angina/syncope occur is 2-3 years in patients with angina/syncope,
and 1-2 years in heart failure without surgery. The mortality of surgery
is < 5%. If coronary disease or LVF is present, it rises to 10-20%.
Calcific aortic stenosis is increasingly common and, due to the
proximity of the atrioventricular node, may be associated with
atrioventricular nodal block, particularly in the post-surgical
population. Emergency treatment: Admit the patient with heart failure
and treat with diuretics.
Aortic sclerosis: The carotid pulse is normal, the apical impulse is just
palpable and not displaced. There are no thrills. There is an ejection
systolic murmur which is not usually harsh or loud and is audible in
the aortic area but only faintly in the neck. The aortic component of
the second sound is well heard. The blood pressure is normal (or
may be hypertensive).
AORTIC INCOMPETENCE
and suggest why.
Symptoms: Dyspnoea is the main symptom. However, initial symptoms
in patients with chronic aortic incompetence often related to the
augmented stroke volume with complaints of a forceful heartbeat
and pulsations in the neck. Angina and syncope are much less common
than in AS. It can be well tolerated if gradual compensation occurs.
Conversely, if the onset is rapid (e.g. dissection or infective
endocarditis), then LVF or CCF can rapidly supervene.
Causes: Primary disease of the valve (congenital valve lesions,
connective tissue laxity as in Marfans syndrome or Hurlers
syndrome), aortic root dilatation and stretching of the valve ring
(hypertensive root dilatation and dissection), or secondary infective
endocarditis, prosthetic paravalvular leak, rheumatic heart disease,
ankylosing spondylitis, cystic medial necrosis, seronegative arthritis,
rheumatoid disease, quaternary syphilitic aortitis (note acute causes
include infective endocarditis, trauma, failure of prosthetic valve, and
rupture of sinus of Valsalva).

Signs: The signs are peripheral signs of increased stroke volume.
Corrigans sign (visible carotid pulsation which may be seen with
harmonious head nodding), Quinkes sign (capillary pulsation of nail
beds), De Mussets sign (head bobbing). Duroziezs sign femoral
diastolic murmur. One may ask the examiner to listen over the femoral
arteries for pistol shots synchronous with the pulse (Traubes sign).
Pulse is regular of good volume and collapsing in nature
(waterhammer). HS normal, apex displaced and forceful, third heart
sound, early diastolic rumbling murmur audible at the left sternal
edge which is loudest with the patient sitting forward in expiration,
ejection-systolic flow murmur across the aortic valve displaced apex
beat towards 5th intercostal space. Carotid pulse has a rapid upstroke
with no dichrotic notch; if the stroke volume is large, there may be a
judder. Systolic blood pressure is usually high.
Signs of severe AR: Wide pulse pressure, soft S2, EDM, S3/left ventricular
failure, Hills sign (systolic bp legs > arms), Austin-Flint (mid-diastolic
murmur at apex) murmur. As the regurgitation becomes more severe,
the length of the murmur increases.
Investigations: ECG (left ventricular hypertrophy/strain and left atrial
hypertrophy), CXR (aortic valve calcification is rare in pure AR, LVH
and venous congestion, the aortic arch may be prominent in
hypertension or dissection, or aneurysmal in Marfans syndrome or
syphilis), echocardiogram (LV function and dimensions, aortic valve
thickening or vegetations, fluttering of the anterior mitral valve leaflet
with prominent mitral valve closure), exercise testing, cardiac catheter
(essential when coronary artery disease suspected and when the
severity of the regurgitation is doubted, anatomy of the aortic root,
LV function, coronary artery and ostial anatomy, other valve disease),
syphilis serology, ANA/rheumatoid factor, sacroiliac XR and HLA
B27 haplotype.
Other causes of a collapsing pulse: pregnancy, patent ductus
arteriosus, Pagets disease, anaemia, thyrotoxicosis.
Treatment: Competitive sport should be discouraged, surgery to halt
volume overload, replace valve (aortic root reconstruction) before
LVESD > 55 mm or concomitant angina/severe AR; nifedipine in
asymptomatics with severe AR, long-term vasodilator not
recommended. In young, metallic prostheses are used as more
durable. The indications for surgery are symptomatic (dyspnoea and
reduced exercise tolerance), or if the following criteria are met: (a)

Pulse pressure > 100 mmHg, (b) ECG changes, (c) Postinfective
endocarditis not responding to medical management, and (d) LV
enlargement on CXR. Ideally replace the valve prior to significant left
ventricular dilatation and dysfunction. Medical management is the
treatment of heart failure and endocarditis prophylaxis.
A REMINDER ABOUT MARFANS SYNDROME

Tall with long extremities (arm span > height; pubis-sole>pubis-vertex).
Arachnodactyly: Can encircle their wrist with thumb and little finger.
Hyperextensible joints: Thumb able to touch ipsilateral wrist and adduct
over palm with its tip visible at the ulnar border.
Face: High-arched palate with crowded teeth.
Eyes: Iridodonesis (with upward lens dislocation)
Chest: Pectus carinatum or excavatum, scoliosis, scars from cardiac
surgery.
Other features: Aortic incompetence (collapsing pulse), mitral valve
prolapse, blue sclerae, underdeveloped muscles, pectus excavatum,
multiple spontaneous pneumothoraces, kyphoscoliosis, aneurysm
tendency, coarctation.
Abdominal: Inguinal hernia and scars.
CNS: Normal IQ.
Differential diagnosis: Homocystinuria (mental retardation and
downwards lens dislocation).
Autosomal dominant, chromosome 15. Defect in fibrillin gene.
Management: Surveillance (monitoring of aortic root size with annual
trans-thoracic echo), treatment with -blockers to slow aortic root
dilatation and pre-emptive aortic root surgery to prevent dissection
and aortic rupture.
MIXED AORTIC VALVE DISEASE

and suggest why.
May have some/all features of both pathologies and the candidate
must determine which lesion dominates.

There may be a bisferiens pulse (notch halfway up the upstroke).
Aortic systolic and diastolic murmurs, maximal down the left sternal
edge.
Determine the dominant lesion: A small volume pulse with a narrow
pulse pressure favours AS; a large volume, collapsing pulse with a
wide pulse pressure favours AR.
Investigations: Echocardiogram (confirms LVH, measures the LV cavity
size and so gives an idea of the severity of regurgitation from the
stroke volume, confirm or exclude the presence of rheumatic valve
disease) and CXR (moderate cardiac enlargement).
Management: The indications for surgery remain the same as that for
pure stenosis or regurgitation.
Table 5.1: Factors pointing to a predominant lesion in mixed aortic valve disease
Pulse
Apex
Systolic thrill
Systolic murmur
Blood pressure
Pulse pressure
Aortic incompetence
Aortic stenosis
Mainly collapsing
Thrusting, displaced
Absent
Not loud, not harsh
High
Wide
Mainly slow rising

Heaving, not displaced much
Present
Loud, harsh
Low
Narrow
MITRAL STENOSIS
and suggest why.
Usual Symptoms
Dyspnoea on exertion, orthopnoea and PND as secondary
pulmonary hypertension develops.
Pulmonary oedema may be precipitated by AF, pregnancy, exercise,
a chest infection or anaesthesia.
Fatiguebecause of the low cardiac output in moderate to severe
stenosis.
Haemoptysis: Alveolar haemorrhage, bronchial vein rupture,
pulmonary infarction because of the low cardiac output and
immobility, bloody sputum with chronic bronchitis due to bronchial
oedema.
Systemic emboli occur in 20-30% of cases, e.g. cerebral, mesenteric,
saddle or iliofemoral.
Chest pain: RVH and normal coronaries.
Palpitations and paroxysmal AF.

Right heart failure with TR and hepatic angina, ascites and oedema.
Dysphagia from left atrial enlargement.
Infective endocarditis is unusual.
Causes: Congenital, rheumatic heart disease, SLE, carcinoid,
rheumatoid disease, malignant carcinoid, left atrial myxoma.
Features: Left thoracotomy scar, atrial fibrillation (irregularly irregular
pulse) or chaotic low volume pulse, malar flush, prominent V wave
in JVP if triscuspid regurgitation secondary to right ventricular
hypertension, undisplaced, tapping apex beat, undisplaced, left
parasternal heave, loud S1, maybe loud S2 if pulmonary hypertension
is present, low-pitched rumbling mid-diastolic murmur loudest at the
apex in the left lateral position in held expiration and accentuated by
exertion, giant v waves due to tricuspid incompetence, signs of
previous valvotomy. Murmur is accentuated by exercise (increase in
heart rate). May be accompanied by early diastolic murmur of
pulmonary regurgitant murmur (Graham-Steel), if there is concomitant
pulmonary hypertension.
Extra points: Haemodynamic significance (pulmonary hypertension,
functional tricuspid regurgitation), endocarditis, embolic complications
(stroke and absent pulses), other rheumatic valve lesions.
Aetiology: Rheumatic valvular disease is by far the commonest cause
Lancefield Group A streptococci cell wall antigens cross react with
the heart valve structural glycoproteins causing inflammation and noncommissural fusion; non-rheumatic disease is very rare, for example,
Congenital: Mucopolysaccharidoses, endomyocardial fibroelastosis,
malignant carcinoid.
Differential diagnosis: Inflow obstruction (left atrial (LA) myxoma, ballvalve thrombus), mid-diastolic murmur can be mimicked by flow
through an atrial septal defect (ASD) but the presence of a widely,
fixed second heart sound, together with the absence of a loud S1,
tapping apex beat and no opening snap in the latter distinguishes the
two conditions; left atrial myxoma; Austin-Flint murmurassociated
with aortic regurgitation (AR), collapsing pulse, volume-loaded
ventricle and early diastolic murmur at the left sternal edge.
Severity determined by signs of pulmonary hypertension and/or
recurrent thromboembolism, shorter interval between S2 and the
opening snap (0.04 0.10 s after opening snap is usual), the longer the
diastolic murmur. A guide to severity on auscultation is: Mild (opening

snap is late around >100 ms after A2), moderate (about 80 ms after
A2) and severe (about <60 ms after A2). A tight stenosis is defined on
area (< 1 cm2).
Tricuspid regurgitation is common in advanced stenosis. The
presence of atrial fibrillation also favours the existence of mitral stenosis.
Evidence of decompensation include pulmonary hypertension,
thromboembolic disease, signs of infective endocarditis, Ortners
phenomenon.
Complications: Left atrial enlargement, pulmonary hypertension, right
heart failure, systemic embolization, tricuspid regurgitation, right
heart failure.
Investigations: ECG (bifid P wave/P mitrale, AF, low voltage in V1,
progressive right ventricular hypertrophy), chest X-ray (congested
upper lobe veins, Kerley B-lines, enlarged left atrium, large carinal
angle, straight heart border, upper lobe diversion, horizontal left main
bronchus), echocardiogram (necessary for differential diagnosis and
to calculate the valve area, as well as to measure the PAP), valve area
and stenosis, transmitral gradient), cardiac catheter (not initially, unless
previous valvotomy, other valve disease, prior to surgery, angina or
valve calcification on the CXR).
Treatment: Medical treatment involves digoxin, verapamil (ratelimiting calcium antagonists), or -blockers andanticoagulation for
AF, diuretics for fluid retention, antibiotics for chest infections,
prophylactic antibiotics for all dental manipulations and potentially
septic procedures, warfarin if previous emboli.
Surgical treatment involves severe symptoms, recurrent emboli,
pulmonary hypertension, pulmonary oedema in pregnancy,
haemoptysis, tight = <1 cm2, percutaneous or open surgical valvotomy,
transvenous balloon valvuloplasty = closed commisurotomy (rather
than mitral valve replacement), prosthetic heart valve, anticoagulation
and antibiotic prophylaxis during procedures, rate control (for atrial
fibrillation). Valvotomy (open or transcatheter) are for mobile valve
and absence of mitral incompetence.
It is embarrassing that, having given rheumatic fever as a cause of
mitral stenosis, candidates sometimes give the impression that they
do not know much about it. Immunological cross-reactivity between
Group A -haemolytic streptococcal infection, e.g. Streptococcus
pyogenes and valve tissue. Duckett-Jones diagnostic criteria. Proven
-haemolytic streptococcal infection diagnosed by throat swab ASOT
or clinical scarlet fever plus 2 major or 1 major and 2 minor: Major:

Chorea, erythema marginatum, subcutaneous nodules (Aschoff
nodules), relapsing polyarthritis (not polyarthralgia), carditis, Minor:
Raised ESR, raised WCC, arthralgia, previous rheumatic fever, pyrexia,
prolonged PR interval.
MITRAL INCOMPETENCE
and suggest why.
Causes: Severe left ventricular dilatation of any cause, rheumatic heart
disease, connective tissue disease, mitral valve prolapse, coronary
artery disease, infective endocarditis, cardiomyopathy, connective
tissue disorders complication of mitral valvotomy, papillary muscle
rupture.
Signs: Chaotic small volume pulse, displaced laterally forceful/
thrusting apex beat, left parasternal heave, apical thrill, soft S1, S3
may be present due to rapid ventricular filling, apical blowing
pansystolic murmur at the apex radiating to the axilla growing through
S2, the loudness of the murmur is of no significance, signs of cardiac
failure.
Extra points: Pulmonary oedema, endocarditis, other murmurs, e.g.
VSD.
Aetiology
Functional (commonly secondary to dilatation of the mitral valve
annulus in severe left ventricular dilatation, either an ischaemic
left ventricle or dilated cardiomyopathy). In elderly,
females>males, calcification of the annulus is seen, this can extend
to involve the cusps, causing MR or it may be benign. It is associated
with diabetes mellitus and Pagets disease and doubles the relative
risk of embolic stroke.
Structural (valvular regurgitation is caused by rheumatic fever or
infective endocarditis).
MV prolapse.
Papillary muscle dysfunction (ischaemia, infarction or other
degenerative disease of the chordae tendinae).
Differential diagnosis: Aortic stenosis, mitral valve prolapse (midsystolic
click), hypertrophic cardiomyopathy, ASD, mitral regurgitation,
tricuspid regurgitation, and ventricular septal defect.

Investigations: ECGP mitrale, atrial fibrillation, left ventricular
hypertrophy + right ventricular hypertrophy; CXRpulmonary
congestion and large heart, echocardiogram: anatomy of mitral valve
apparatus, LA and LV size and function; cardiac catheter needed to
confirm the diagnosis, and for coexistent coronary artery or aortic
stenosis disease, size of jet, vegetations or ruptured papillae. The LA/
pulmonary wedge V wave pressure gives a measure of severity.
Severity: Larger left ventricle dilated with a displaced thrusting apex,
S3.
Complications: LV failure, AF, infective endocarditis, pulmonary
hypertension, RV failure, thromboembolism, sudden death.
Treatment: Management of AF with digoxin, antibiotic prophylaxis
during procedures followed by serial echos, digoxin to slow
ventricular response, anticoagulation is withheld unless there is a
history of emboli, prosthetic MVR or coexistent MS with a low cardiac
output, treatment of heart failure though diuretics (to decrease
pulmonary venous congestion and LV preload) and ionotropes.
Acute MR is managed as cardiogenic shock-sodium nitroprusside
reduces afterload.
Major consideration should be given to surgery if LVEF < 55
60% or patients with enlarging left ventricular dimensions, and a
threshold LVSD and cardiomegaly despite medical therapy.
Moderate to severe symptoms (NYHA III/IV should be offered
surgery provided left ventricular function is adequate, or NYHA II
and LV enlargement on CXR, or increasing dyspnoea. Valve repair
(preferable) or replacement. Aim to operate when symptomatic, prior
to severe LV dilatation and dysfunction.
If surgical repair is possible, it should be considered in all patients
< 75 years who have a flail leaflet or persistent AF.
Prognosis: Often symptomatic for > 10 years, mortality 5% per year in
symptomatic patients. 60% of patients with chronic MR are alive at 10
years. Prognosis depends on the LV function. Poor prognostic features
are symptomatic history at < 1 year, AF, > 60 years of age, LVEF <
50% dilated LV, and echo LV size at end-systole > 5 cm, end-diastole
>7 cm.
MIXED MITRAL VALVE DISEASE

and suggest why.

May have some/all features of both pathologies and the candidate
must determine which lesion dominates.
Determining the dominant lesion:
AF favours MS rather than MS but the latter can also cause AF.
Raised JVP.
Left parasternal heave is present.
Loud S1 and tapping apex favours MS.
Soft S1 favours MR.
Opening snap is either soft or absent.
Mitral regurgitation causes the pansystolic murmur.
The delayed diastolic murmur is not of full length, but may be
loud, or even palpable indicating the increased left ventricular stroke
volume.
May have ankle oedema or even ascites due to fluid retention,
although these are rather unusual in the absence of tricuspid
regurgitation.
The presence of S3 suggests that accompanying MS is not severe.
Features of pulmonary hypertension (malar flush; loud P2;
accompanying TR; Graham-Steel murmur) favours MS rather than
MR.
Investigations
ECG: AF, LVH
Echocardiogram: Reduced diastolic closure rate with anterior movement
of the posterior cusp during diastole confirms the presence of
rheumatic valvular disease. Left ventricular cavity size may be
increased. The extent of disease of the valve cusps and subvalve
apparatus is apparent.
CXR: Cardiomegaly with selective enlargement of the left atrium. In
mixed mitral valve disease, the LA may be very large with a volume
up to three litres. The lung fields may show similar changes to those
of pure mitral stenosis.
Management: Valvotomy/valvuloplasty is unlikely to be appropriate.
Mitral valve replacement is probable.
Dominant abnormality: Mitral stenosis small volume pulse, nondisplaced/tapping impulse, loud S1, absent S3. Mitral incompetence
small abbreviated pulse, displaced thrusting apex, loud S1, S3 present.

Table 5.2: Factors pointing to a predominant lesion in mixed mitral valve disease
Pulse
Apex
First heart sound
Third heart sound
Mitral stenosis
Mitral incompetence
Small volume
Not displaced; tapping impulse
present
Loud
Absent
Sharp and abbreviated

Displaced; thrusting
Soft
Present
MIXED AORTIC AND MITRAL VALVE DISEASE

and suggest why.
Most commonly mitral regurgitation together with aortic stenosis.
MR with mid/late systolic murmurs may mask the AS murmur.
If the apex beat is displaced, MR dominates.
Tricuspid Incompetence
Examine this patients cardiovascular system. He has been
complaining of abdominal discomfort.
Symptoms: Abdominal discomfort and distension; hepatic angina;
jaundice; peripheral oedemal fatigue and dyspnoea.
Examination: Pulse chaotic and of low volume, V waves or giant systolic
CV waves in the JVP, right ventricular/left parasternal heave,
palpable S2, atrial fibrillation, pansystolic murmur at LSE louder on
inspiration, S3, hepatic pulsation, ascites, peripheral oedema including
ascites and ankle oedema. One must proceed to examine the lungs for
a cause of pulmonary hypertension (and features, including RV heave,
loud P2), as well as the abdomen and beyond, for the peripheral signs
of tricuspid regurgitation: Peripheral and central cyanosis, ascites and
other signs of chronic liver disease, tender pulsatile hepatomegaly,
peripheral oedema.
Important to look for multiple venepuncture sites (mainline drug
addiction) and facial telengectasias (carcinoid syndrome).
Aetiology: Functional (secondary to pulmonary hypertension), organic
(infective endocarditis, floppy tricuspid valve associated with a floppy
mitral valve associated with congenital heart disease), rheumatic
tricuspid valve disease in association with aortic and mitral valve
area; right sided endocarditis; right ventricular infarction;
endomyocardial fibrosis; rarer causes include carcinoid syndrome and
secondary to the centrally acting appetite suppressants phentermine,
fenfluramine and dexfenfluramine all of which have been withdrawn.

Investigations: ECG AF, P pulmonale and RV hypertrophy;
echocardiogram dilated or hypertrophic RV, functional TV disease,
vegetations, magnitude of regurgitant jet on Doppler
ultrasonography; cardiac catheter.
Management: Management of the underlying lung disease, diureics,
fluid restriction, surgery, annuloplasty and plication, valve replacement
(rarely).
MITRAL VALVE PROLAPSE

This young lady is short of breath.
Please examine her cardiovascular system and suggest why.
Mitral valve prolapse is most prevalent in young females who
present with atypical chest pain or paroxysmal arrhythmias.
Common especially in tall young women.
Common, 210% population, associated with Marfans syndrome.
Ehler Danlos, rheumatic heart disease, ostium secundum, ASD, EhlerDanlos/pseudoxanthoma elasticum, psoriatic arthropathy, congenital
heart disease, congestive cardiomyopathy, HOCM, myocarditis, mitral
valve surgery, Fabrys disease, osteogenesis imperfecta, SLE, Ebsteins
anomaly.
Pulse may have ectopics.
Apex is undisplaced, normal character.
Murmur is a systolic mid- or even pan-systolic; the clicks may be
multiple and there may be a systolic squeak or honk at the apex. With
posterior leaflet prolapse the murmur may radiate to the left sternal
edge.
The duration of the murmur is reduced by short squatting exercises
(the click is brought closer to S2), and increased by standing from
squatting or performing a Valsalva manoeuvre. This decreases the
cardiac volume and as a result the click and murmur occur earlier
during systole and the murmur is prolonged. Increasing cardiac
volume (squatting) has the reverse effect.
ECG may show T wave inversion.
Complications: Small risk of emboli, severe mitral regurgitation,
arrhythmias, atypical chest pain, TIAs, infective endocarditis, sudden
cardiac death. Rx: Reassure asymptomatic patient, prophylaxis if
murmur, atypical chest pain treat with painkillers or -blockers, aspirin
for TIAs, antirhythmics, endocarditis prophylaxis. Palpitations are
usually due to benign ventricular ectopy and generally respond well
to beta blockade if symptoms are troublesome.
PULMONARY HYPERTENSION
This woman is short of breath, and has been reported by her GP as
having a blood pressure around 90/55 most of the time. Please examine
her cardiovascular system and suggest why.
Presentation is usually with dyspnoea, fatigue, syncope, oedema,
palpitations; in the discussion offer a discussion without offending
the patient for OCP and fenfluramine, HIV history; large a waves
JVP, left parasternal heave, loud P2, ejection click in the pulmonary
area, early diastolic murmur. CXR: Enlarged pulmonary arteries; ECG:
RVH, right atrial hypertrophy. VQ scan to exclude thromboembolic
disease. Echo. Rx: Diuretics, anticoagulants, prostaglandins, sildanefil.
PULMONARY STENOSIS
This patient has a long standing cardiovascular problem, but he is
generally well. Please examine his chest and report your findings.
Extra points: Noonans syndrome: Phenotypically like Turners
syndrome but male sex, other valve lesions, right ventricular failure
(ascites and peripheral oedema). Noonans syndrome is on 12q24.
Other aetiological factors: Rheumatic fever, carcinoid syndrome.
PR invariably results from dilatation of the pulmonary annulus,
which may occur with pulmonary hypertension. RVH and right atrial
hypertrophy may develop.
Both mild PS and mild PR are asymptomatic. More severe disease
may present with a low cardiac output and right heart failure.
Clinical signs: Raised JVP with giant a waves, left parastenal heave,
thrill in the pulmonary area. Auscultation reveals an ejection systolic
murmur loudest in the pulmonary area in inspiration. Pulmonary
regurgitation is characterized by a decrescendo early diastolic murmur
in the pulmonary area (Graham-Steell murmur).
Investigation: ECGnormal, p pulmonale, RVH, RBBB, CXR oligaemic
lung fields and large right atrium, TTEgradient calculation.
Management: Pulmonary valvuloplasty, pulmonary valvotomy, if
gradient > 70 mmHg or there is RV failure.
POOR LV FUNCTION
and suggest why.

Hypertension, fluid retention, cold clammy skin, low blood
pressure, displaced apex beat, right ventricular heave; aetiology
valvular disease, hypertension, atherosclerosis, severe anaemia,
pathological arrhythmia, generalized myopathy. Ix: CXR, echo. ECG:
cause, left ventricular hypertrophy, arrhythmia, pathological Q waves.
Blood tests for associated renal/liver disease, metabolic causes,
thyroid, sarcoid, amyloid (electrophoresis, rectal biopsy), nuclear
imaging. 24 Holter for ventricular arrhythmia.
Congestive cardiac failure is a cause of a raised JVP. Other causes
are cor pulmonale, pulmonary hypertension, constrictive pericarditis,
and a large pericardial effusion.
CONGENITAL HEART DISEASE

The congenital heart diseases are:
Basic classification of congenital heart disease
Cyanotic
Acyanotic
Tetraology of Fallot
Eisenmengers syndrome
Transposition of the Great Arteries
Ebsteins anomaly
Atrial septal defect

Ventricular septal defect
Patent ductus arteriosus
Coarctation of the aorta
The following are complications of chronic cyanosis:

1. Polycythaemia causing hyperviscosity symptoms
2. Abnormal haemostasis and haemorrhagic risk
3. Paradoxical embolism causing cerebral abscess or stroke.
ACYANOTIC HEART DISEASE

Ventricular Septal Defect
This 26-year-old lady was found to have a murmur on routine
examination by her GP. Please examine her cardiovascular system
and suggest your management.
Symptoms: Small VSDs are common and asymptomatic. As pulmonary
hypertension develops, fatigue, dyspnoea and symptoms of right
ventricular failure occur.
Pulse: Normal
Left parasternal heave (if there is RV enlargement).
Absence of the normal splitting of S1 suggests that the left and
right ventricle pressures are equal.
A loud, harsh pansystolic murmur and associated thrill at the left
sternal edge should also be heard.

Perhaps mid-diastolic murmur at the apex due to high flow through
the mitral valve.
As VSD becomes larger, both left and right ventricular
hypertrophy occur and the pulmonary arteries may become palpable.
Both the murmur and the thrill become softer. The jet veloity of the
VSD and the pressure gradient between the ventricles is smaller, the
larger the defect. As pulmonary hypertension becomes prominent
the murmur may disappear as the ventricular pressures equalise.
Eventually, Eisenmenger complex (a right-to-left shunt) may develop.
Extra points: Other associated lesions: AR, PDA (10%), Fallots
tetraology and coarctation.
Pulmonary hypertension: Loud P2 and RV heave.
Shunt reversal: Right to left (Eisenmengers syndrome), cyanosis and
clubbing.
Feaures of endocarditis.
Causes: Congenital, or acquired (post-MI). May be associated with a
syndrome (tricuspid atresia, pulmonary atresia, transposition of the
great arteries, coarctation), or be an integral part of the syndrome
(Fallots tetraology, double-outlet right ventricle, truncus arteriosus).
Differential diagnosis: Mitral valve regurgitation, AS, HCM, tricuspid
regurgitation, PS.
Investigations: ECG (LAH, left or right ventricular hypertrophy in a
large defect), CXR (cardiomegaly, pulmonary plethora, prominent
pulmonary arteries in a large defect as pulmonary plethora),
echocardiogram for pressures and cardiac catheter for oxygen
saturations.
QRS axis may shift to the right in pulmonary hypertension.
The pulse volume may be small if there is a large left-to-right shunt.
Magnetic resonance scanning can demonstrate the defect and enable
the shunt to be measured. Catheterisation confirms the step-up in
oxygen saturation in the RV, quantitates the shunt, and diagnoses the
site. Aortography will check the valve and exclude PDA or coarctation.
RV angiography checks the RV outflow tract.
Complications: Endocarditis (possibly recurrent; look for splinter
haemorrhages), biventricular cardiac failure, aortic regurgitation,
pulmonary hypertension eventually leading to Eisenmengers
syndrome.

Treatment: Surgery, if a large defect with a pulmonary: Systemic flow
of >2:1 and right ventricular overload, medical therapy has failed,
symptomatic +++ or infective endocarditis; patients who survive to
adulthood usually have left ventricular failure or pulmonary
hypertension with associated right ventricular failure. Surgical closure
of such defects is recommended. Medical treatment: Many (30-50%)
small VSDs close spontaneously, and although the surgical morbidity
and mortality surrounding correction of small defects is low, surgery
is usually unnecessary; all types require IE prophylaxis, there are septal
closure devices available that may be placed at the time of cardiac
catheterisation. Post-MI VSDs require urgent surgery.
Note on congenital heart disease: Acyanotic heart disease: ASD, VSD,
Aortic coarctation, PDA; Cyanotic: Fallots (VSD with right to left
shunt, pulmonary stenosis, RVH, aorta overriding septal defect),
Transposition of Great Arteries, Eisenmengers syndrome. A small
defect may produce a loud murmur (Maladie de Roger). Eisenmenger
centrally clubbed and cyanosed, left parasternal heave, palpable
pulmonary valve closure.
ATRIAL SEPTAL DEFECT

This young woman complains of cough and occasional palpitations.
Examine her cardiovascular system.
Features: Presents with dyspnoea, productive cough indicating
recurrent pulmonary infections, symptoms of paradoxical emboli,
palpitations (indicating atrial arrhythmias), fatigue and ankle swelling
(indicating heart failure).
Examination: Diffuse or normal apical impulse, left parasternal heave
(prominent right ventricular impulse), ejection systolic flow murmur
in left second and third intercostals space, wide fixed split second
heart sound, atrial fibrillation, A and V waves in raised JVP.
Look for signs of pulmonary hypertension (Eisenmenger complex:
Centrally cyanosed and clubbed; pulse volume usually small; second
heart sound is loud and single, there may be a right ventricular fourth
heart sound). When an ASD is suspected, go onto carefully listen for
a murmur of mitral stenosis which, if present with ASD, is called
Lutembachers syndrome.
Types of ASD: Ostium secundum defect accounts for around 70% of
cases, and the defect is in the middle portion of the atrial septum.

Primum is nearest the atrioventricular valve apparatus. ECG often
shows right axis deviation and incomplete right bundle branch block.
CXR demonstrates prominent pulmonary arteries (large pulmonary
conus) and shunt vascularity, progressive aortic enlargement, small
aortic knuckle. ECG: Right axis deviation, RBBB (left axis deviation in
ostium primum defects), atrial arrhythmias. Echocardiogram: Microbubble contrast is used to visualize shunting.
Complications: Atrial arrythmias (atrial fibrillation is most common),
pulmonary hypertension, paradoxical embolus, infective endocarditis
(in patients with ostium primum defect only), recurrent pulmonary
infections, Eisenmenger syndrome with reversal of shunt. Management:
Surgical closure between 5 and 10; in adults, small ASDs can be left
alone but large shunts large enough to give clear physical signs should
be closed.
Management: Drug treatment has a role only in the management of
the complications of the defect such as atrial fibrillation (digoxin),
right ventricular disease (diuretics), and infective endocarditis
(antibiotis). Umbrella devices may be placed at the time of cardiac
catheterisation. Left-to-right shunt saturations of 1.5:1 or more require
surgical closure to prevent right ventricular dysfunction. Otherwise,
ostium secundum ASDs whilst having been traditionally closed in or
before the third decade may be little gained from surgery in
asymptomatic adults.
Associations: Downs syndrome: Endocardial cushion defect causes a
primum ASD and other atrioventricular valve abnormalities.
COARCTATION OF THE AORTA

This man is hypertensive. Please examine his cardiovascular system
and suggest why.
Large volume asymmetric pulses, vigorous carotid pulsation,
radiofemoral delay, ejection systolic murmur loud posteriorly over
the praecordium, visible scapular collaterals, visible arterial pulsations
and bruits over scapulae and anterior axillary areas and left upper
thorax in general, heaving/thrusting apex due to left ventricular
hyptertrophy. Request permission to take blood pressure
measurements in upper and lower limbs. Coarctation is usually distal
to the left subclavian artery near the insertion of ligamentum
arteriosum. Early clues to the lesion on inspection may be greater
development of the upper extremities and thorax than the lower
extremities.

Associations: Cardiac: VSD, bicuspid aortic valve and PDA; Non-cardiac:
Turners syndrome and Berry aneurysms.
Decompensation: Hypertension and its consequences, bicuspid aortic
valve, cerebral aneurysms, infective endocarditis.
Investigations: ECG LVH, CXR rib notching, dilated descending aorta,
a figure of three sign due to indentation of the aorta of the site of
coarctation with pre- and post-stenotic dilatation. Note that rib
notching is not a specific sign as it may occur in neurofibromatosis or
inferior vena cava obstruction. Echo: Visualize.
Treatment: Treatment for transcoarctal pressure > 30 mmHg through
balloon dilatation/surgical resection. Hypertension may continue after
surgery.
Patent Ductus Arteriosus

This patient is to have a routine dental extraction. Examine his
cardiovascular system, and suggest whether any precautions need to
be taken.
Definition: Aortopulmonary shunt, high to low pressure, with a
continuous machinery pansystolic murmur due to increased blood
flow through the lungs best heard at the end of systole in expiration
which may preclude S2, radiating to the left clavicle and heard
posteriorly, location left upper sternal edge, associated thrill in the
second intercostal space, large defects may be associated with a
collapsing pulse, apex displaced inferolaterally,
History: Low birth weight baby, baby born prematurely, baby borne
at altitude, 1st trimester rubella in mother.
Symptoms: If small, picked up routinely or coincidentally in a well
pink thriving child. If large shunts, they become systematic with heart
failure.
Differenetial diagnosis: Pulmonary AV fistulas, coronary AV fistulas,
venous hum (young children), MR and AR, VSD with AR.
Investigations: ECG N or LVH, CXR normal or left ventricular/left
atrial enlargement, echocardiogram to visualize DA, cardiac catheter.
Common complications: Heart failure, infective endocarditis, pulmonary
hypertension, death, rupture. Signs of decompensation: Untreated
pulmonary hypertension, Eisenmengers complex.

Treatment: Infective endocarditis is extremely rare on very small PDAs
and these can be left alone. Larger PDAs need treating to avoid
failure and endocarditis. Medical therapy is necessary to treat failure
(which can occur for the first time in adult life). Definitive treatment
is with ligation or duct occlusion: many of the problems of ligation
have been obviated by the use of duct occluders implanted in patients
in the catheter laboratory. Irreversible pulmonary hypertension
causing Eisenmengers syndrome is rare, around 5%.
CYANOTIC HEART DISEASE

Eisenmenger Syndrome
This young woman aged 26 has had learning difficulties. Please
examine her cardiovascular system and comment on her potential
management.
Symptoms: Failure to thrive, impaired growth, intellectual impairment
(if severe).
Limited exertional dyspnoea, haemoptysis and frequent chest
infections are symptoms of cyanotic heart disease.
Cerebral abscesses, paradoxical emboli, polycythaemia, bleeding
diathesis and gout occur.
Signs
Centrally cyanosed and plethoric,

Digital clubbing,
Pulse regular and small volume,
Venous pressure normal (or raised if RV failure has developed)
and the a wave is prominent (the atria are contracting against a
raied RV pressure); there may be a prominent V wave (if tricuspid
regurgitation).
Left parasternal heave.
Pulmonary arteries may be palpable, as may P2.
There is no thrill (there is insufficient pressure differential to create
one). S2 - single and loud (pulmonary hypertension has developed,
thus P2 is loud); there may be a (right ventricular) P2.
Possible pansystolic murmur over the tricuspid area (TR, if the
valve cusp has been dilated consequent upon RV failure), as well
as an early diastolic murmur over the pulmonary valve (similarly,
PA dilatation causing PR the Graham-Steell murmur).
Aetiology
Large non-restrictive ventricular septal defect (a single S2),
Primary pulmonary hypertension,
Atrial septal defect (S2 is widely split and does not vary with
ventilation A2 precedes P2; P2 does not move, as the increased
stroke volume does not vary with ventilation),
Patent ductus arteriosus (S2 is normal, i.e. A2 precedes P2 and P2
moves with ventilation; there may be differential cyanosis, pink
fingers and blue, clubbed toes).
Other complex congenital heart disease,
Fallots tetraology.
A palliative procedure involving redirection of the venous return
has been successful in the presence of the great arteries, VSD and
severe pulmonary vascular disease.
Investigations: FBC polycythaemia; ECG: P pulmonale, RAD, tall R
waves, inverted T waves in the right precordial leads (right ventricular
strain pattern), atrial arrhythmias; CXR: PA dilatation, pruning of the
peripheral vessels, prominent pulmonary arteries; echocardiogram
underlying anatomical defect will be localized, flow seen with Doppler
ultrasonography; catheter measures PA pressure and looks for
evidence of right-to-left shunting. The response to pulmonary
vasodilators should be tested.
Management: If Eisenmengers syndrome has developed, it is too late
for correction of the cardiac anomaly. As a consequence of the increased
pulmonary blood flow, the pulmonary vascular resistance rises. When
the pulmonary pressure exceeds the systemic pressure, the left-toright shunt reverses to become right to left, and Eisenmengers
syndrome develops. Heart-lung transplantation offers the only hope
for a few young selected patients. Give endocarditis prophylaxis.
Pregnancy should be avoided. Perform venesection to keep the
haematocrit below 0.45. Avoid anticoagulants. A poor prognosis is
associated with syncope, signs of RV failure, low cardiac ouptut and
severe hypoxaemia.
TETRALOGY OF FALLOT
and suggest why.
This is an acyanotic congential heart disorder which comprises
four separate defects.
Ventricular septal defect with reversal of the shunt

Right ventricular hypertrophy
Pulmonary stenosis
Aorta that overrides the VSD.
Signs: Cyanosis, clubbing, RV heave, inaudible P2, normal S1.

Investigations: ECG (right ventricular hypertrophy and R-axis
deviation), CXR (boot shaped heart).
Complications: Ventricular arrhythmias, AF or atrial flutter, pulmonary
regurgitation, recurrent VTOTO.
Eisenmengers syndrome is the reversal of flow through a shunt,
resulting in cyanosis as the pressures from the right heart exceed
those of the left heart. This is most often seen in the context of shunts
through VSDs, e.g. in Tetralogy of Fallot but can occur in any shunt
situation.
Blalock-Taussig shunts: Corrects the Fallots abnormality by
anastamosing the subclavian artery to the pulmonary artery. Currently
complete surgical correction is standard.
Other causes of an absent radial pulse. Acute: Embolism, aortic
dissection, trauma, e.g. cardiac catheter, and death. Chronic:
Coarctation, Takayasus arteritis.
TRANSPOSITION OF THE GREAT ARTERIES

This man is quite short of breath. Please examine his cardiovascular
system and suggest why.
The aorta arises anteriorly from the right ventricle (the systemic
ventricle) and the pulmonary artery from the left (so the two
circulations are separate). A communication (foramen ovale, patent
ductus arteriosus or septal defect) between them is necessary for
survival.
Clinical presentation is with cyanosis from birth, and LVF in infancy
if the left-to-right shunt is large.
Signs are of cyanosis and a single loud S2.
The ECG may show right axis deviation and RVH. Look for
cardiomegaly and increased pulmonary vascularity on the chest
radiograph.
The treatment was previously by atrial switch (venous returns are
re-routed through the atria). Currently, treatment is by arterial switch
in neonates.
EBSTEINS ANOMALY
This man was found have an enlarged liver clinically, later verified
on ultrasound. Please examine his cardiovascular system and suggest
why.
The tricuspid valve is displaced into the right ventricle, leaving a
small functional ventricle. 80% of these have a ASD or PFO and a
right-to-left shunting occurs if the right atrial pressure rises.
There is a wide spectrum of presentation, from incidental finding
to severe venous congestion and cyanosis.
Signs: Cyanosis, tricuspid regurgitation, hepatomegaly.
Investigations: ECG tall/broad P waves, RBB, first-degree heart block,
delta wave.
Treatment: Diuretics and digoxin for LV failure, anti-arrhythmics or
ablation for arrhythmics and tricuspid repair/replacement and surgical
closure of ASD.
Complications: Atrial arrhythmias and/or accessory pathways (WolffParkinson-White syndrome).
Central Nervous
System (Station 3)

This title of this station is really a misnomer, as much of the station
potentially can focus on the peripheral nervous system. Anyway,
neurology appears to be everybodys favourite nightmare. It becomes
easy when approached in a logical fashion, but practice is required,
and you must fulfil the requirements of the task within the time
allowed.
Tips for the Examination

Always introduce yourself properly.
Ask the patient if he/she is comfortable, and ask whether or not
he/she is in pain before you touch the patient regardless of what
you are about to examine.
Always adequately expose the patient, e.g. if you are to examine
the upper limbs ensure that jumpers and shirts are removed to
expose the entire limb including the shoulder girdle.
Position the patient in the correct position.
Ensure that there is adequate lighting.
Observe the surroundings, e.g. look for the wheelchair, walking
stick, glasses.
Examination of the Limbs

The approach to the examination should always be systematic and
methodical. Regardless of what you think the diagnosis is, you have to
approach all cases systematically. This will demonstrate that you can
demonstrate the signs to your examiner and also it is important that
you do not miss other pathology. Approaches to the neurological
Central Nervous System (Station 3)
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differential diagnosis include: Pattern recognition inferred from a

specific constellation of symptoms and signs requires accurate recall
of details; hypothesis testing such that from a patients initial complaints
a diagnostic hypothesis is generated; and anatomical diagnosis, i.e. the
site of the lesion with a pathological differential diagnosis (the advantage
of this approach is that it requires basic knowledge to organise the
signs and symptoms into the major anatomical systems involved. The
neurological findings become manageable, when put into the appropriate
anatomical compartments: Upper motor neurone (UMN), lower motor
neurone (LMN), root lesion, nerve lesion, neuropathy (distal
distribution), myopathy (proximal distribution). Neurology requires a
good understanding of the functional anatomy of the nervous system.
Figure 6.1
COMMON FOCAL NEUROLOGICAL SIGNS AND

THEIR LOCALISATION
A lot of neurology, like the rest of medicine, is pattern recognition.
The summary Table 6.1 gives some common neurological signs and
their localisation.
Table 6.1: Pattern recognition in neurology
Hemiparesis and facial weakness,
Contralateral hemisphere
hemisensory loss, aphasia, or hemianopia
Hemiparesis without any other findings
Lacunar infarct pons/contralateral hemisphere
Hemiparesis with contralateral

cranial nerve
Brainstem
Bilateral pain and temperature loss,

LMN signs level of the lesion sacral
sparing
Central cord syndrome
Hemiparesis with contralateral loss of

pain and ipsilateral loss of vibration
and position sense
Hemicord syndrome (Brown-Squard

syndrome)
Contd...

Contd...
Bilateral motor weakness and loss of
pain and temperature-sense, sparing
vibration and position-sense
Anterior cord syndrome
Bilateral loss of vibration and

position sense
Posterior columns
Paraparesis
At or below thoracic cord parasagittal lesions
Monoparesis (most muscles of a limb)
Brachial or lumbar plexus, exclude cerebral

infarct
Loss of pain and temperature in a saddle Conus medullaris

distribution, sphincter and sexual
dysfunction/motor signs
Bilateral, asymmetrical motor and
sensory loss L & S segments, sphincter
and sexual dysfunction
Cauda equina syndrome
Weakness of isolated muscles
Spinal root lesion or peripheral neuropathy
Bilateral distal numbness + weakness

reflexes
Peripheral neuropathy
Bilateral proximal limb weakness w/o

sensory signs
Muscle / NMJ / GBS
PHYSICAL EXAMINATION
In examination of the upper or lower limbs, the marksheet explicity
states that the candidate should assess motor function in limbs
(including tone and power) and sensory function (including pinprick,
vibration sense, propioception and temperature), as well as
coordination and cerebellar function.
APPEARANCE
Appearance of the limbs is very important.
Look for evidence of muscle wasting and hypertrophy look at
all the muscle groups: note any atrophy or dystrophy and whether
this is generalaised (systemic cause) or focal (localised cause), proximal
(muscle disease) or distal (conduction problem peripheral nerve/
root). Muscle wasting tends to be symmetrical in the case of a muscle
disorder.
Look for any evidence of deformity, there may be deformity as a
result of neurological imbalance, with gross discrepancies in the size
of limbs (infantile hemiplegia, childhood polio). The pseudohypertrophy seen in both Duchenne and Becker muscular dystrophy
is due to replacement of muscle by fatty/fibrous tissue. The classical
inverted champagne bottle (greater muscle loss distally than
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proximally), appearance attributed to hereditary sensorimotor

neuropathy be seen in any longstanding peripheral neuropathy, as
can the often co-existent pes cavus and hammer toe deformities (also
Refsums disease and Fredreichs ataxia). The deformity of a spastic
upper motor neurone syndrome should not be missed (flexed upper
limb, extended lower limb), as often this sole finding when unilateral
puts the site of the pathology within the cerebral cortex.
Look for fasciculation: Look closely at the thigh and deltoid muscle
groups for any twitching or fasciculation (look for at least 30 seconds).
Elicit any pronator drift: Ask the patient to hold out their arms in
front, with the palms facing the ceiling. If the arm starts to dtift (often
first) and pronate, there is a high chance of detecting other signs of
an upper motor neuron (UMN) syndrome.
TONE, POWER, REFLEXES AND COORDINATION

Tone: Tone is resistance to passive movement at a joint.
Two ways of checking it in the legs:
1. Lift up the knee quickly and watch the foot: If there is increase in tone,
the heel will lift off the bed, as the knee does not bend. A lot of
people argue that this is an unpleasant way of testing, and if there
is a diabetic ulcer on the heel.
2. Roll the whole leg backwards and forwards and watch the foot: The foot
should flop at the ankle. With increased tone it moves as a stiff
extension of the lower leg.
Two types of increased tone:
Spasticity: UMN sign of pyramidal tract damage. Commonest form
seen after the stroke. Resistance is high in the early range of movement,
but eases suddenly when this is (gently) overcome.
Rigidity: Extrapyramidal sign, virtually always related to Parkinsons
disease. Resistance is maintained throughout the range of movement,
a bit like bending a lead pipe (which we do regularly in our
department). If there is associated tremor, this results in
cogwheeling. Best tested at wrist and elbow simultaneously. There
is waxy resistance to passive movement, which is maintained
throughout the range of movement.
Clonus: It is easiest to perform the test for clonus at this stage for two
reasons. Firstly, if present, it implies there is an upper motor neurone
problem and hyper-reflexia should be present and secondly it is often
forgotten about, if left until later to perform. Clonus is best elicited at
either ankle or knee joint.
MRC Classification of Power

This is a subjective assessment. Be gentle and compare the
corresponding groups of both sides before moving to the next group,
i.e. left biceps, right biceps, left triceps, right triceps, etc. Ideally you
should test the patients dominant and therefore stronger side with
your dominant side.
0 no movement,
1 flicker/fasciculation,
2 movement on the bed surface but no anti-gravity power,
3 anti-gravity power but no more (cannot overcome resistance),
4 reduced power against resistance,
5 normal power, for all the major flexor/extensor pairs as well as
small muscles of the hand.
It will be expected that, at any point during the examination, the
examiners may ask the candidate for the muscle being tested, the
root value and the action of that particular muscle.
Upper Limbs
Hold your arms out to your sides. Now keep them up. Deltoids C5
Shoulder abduction.
Now push them in towards you and dont let me stop you.
Pectoralis C6, 7, 8 Shoulder adduction.
Pull your arms up towards you and dont let me stop you. Biceps
C5 Arm flexion.
Now push me away Triceps C7 Arm extension.
Clench your fists and bend your wrists up towards you Wrist
flexors C7.
Now push the other way Wrist extensors C7.
Put your hand down flat like this and point your thumb towards
your nose. Now, keep it there and dont let me push it down Abductor
pollicis brevis/Median nerve C8/T1.
Spread your fingers wide apart and dont let me push them
together. Finger abduction/dorsal interossei/ulnar nerve. T1
Now hold this piece of card between your fingers and dont let
me pull it away. Finger adduction/palmar interossei/ulnar nerve
T1.
Reflexes - with the tendon hammer held perpendicular to the line
of the tendon, strike the tendon gently by holding the hammer by its
length. The reflexes should be graded against the MRC standard 0
areflexia, 1 with reinforcement only, 2 physiological, 3
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hyperreflexive, 4 clonus. Plantar response: The Babinski response is

present, if a contraction in the quadriceps is seen, even if the toes
dont fan or extend.
Upper limbs: Biceps C5/6, Supinator C5/6, Triceps C7.
Coordination: If performed early, valuable information can be
sought even before power is assessed. This is particularly useful, as
occasionally the examiner will cut short your examination if he/she
feels that too much time has been taken up by power assessment and
an assessment of coordination cannot even be made. However, it is
extremely unlikely that an examiner will ask you to finish prior to
assessing the power. Secondly, if the patient is unable to lift his arm
or leg in order to assess coordination, then all that remains to be
done when assessing power, is to determine to what degree the loss
of power is. In the upper limb, perform the finger-nose test and in the
lower limb perform the heel-shin test.
Lower Limbs
Im going to test the strength of some of the muscles in your legs.
Keep your leg straight and lift it up into the air. Now, keep it up and
dont let me stop you. Hip flexion. L1,2. Iliopsoas.
Now push your leg down into the bed and dont let me stop
you. Hip extension. L4,5. Gluteus.
Push out against my hand. Hip abduction. Glutei. L4,5.
Push in against my hand. Hip adduction. Adductor group. L2,3,4.
Bend your knee and pull your heel up towards you: dont let me
stop you. Knee flexion. Hamstrings. L5,S1.
Now straighten your knee out. Knee extension. Quadriceps. L3,4.
Pull your foot up to you and dont let me stop you. Ankle
dorsiflexion. Tibialis anterior and long extensors. L4,5.
Push your foot down against my hand. Ankle plantar flexion.
Gastrocnemius. S1.
Push your foot out against my hand. Eversion of foot. Peroneus.
S1.
Push your foot in against my hand. Inversion of foot. Tibialis
anterior and posterior. L4.
Reflexes: See above.
Lower limbs: Knee L4, Ankle S1.
Coordination: See above.
SENSORY TESTING
It is important that you are confident about the dermatome distribution
in the upper and lower limbs, bearing in mind that the clearest
delineation is distally, rather than proximally, and that you are clear
in your instructions to the patient.

For this reason, start distally and assess sensation (start with the
orange stick if available, rather than your finger) in the dermatome
distribution, working your way proximally. Explain Im going to
move this down your arms/legs, tell me if it feels sharp/soft, then
say now shut your eyes, compare one dermatome on the right with
the corresponding one on the left, and move down the dermatomes
try to define the sensory level or glove and stocking peripheral
neuropathy. Useful levels are: T4 nipple, T10 umbilicus, T12
above the inguinal ligament, and L1 below the inguinal ligament.
Test pinprick sensation using appropriate sharps which do not
penetrate the skin. Pinprick sensation using appropriate sharps which
do not penetrate the skin. Also remember to check the back of the
patient to determine whether the abnormality is actually dermatomal
or not.
If you are asked to examine to perform a sensory neurological
examination of the lower limbs, the first thing is to rule out is a
peripheral neuropathy.
Cotton-wool to touch and not drag the stimulus along the surface
of the skin. I want you to say YES if you feel me touch you with this
piece of cotton wool. Avoid hairs on legs where you can, tickle is
transmitted in the spinothalamic tract.
Joint position sense: Upper limb drift with eyes closed. Im going
to move your finger up and down; this is up and this is down. Now
close your eyes and tell me whether I am moving your finger up or
down.
Place a ringing tuning fork on the superior aspect of the manubrium.
Establish what the patient recognises as normal (i.e. reference at the
top of the manubrium sterni), and ask him/her to confirm whether
they next feel the same again. Start distally on bony prominences: For
the legs, 1st MTP joint (bunion), medial malleolus, tibial protuberance
(knobble below patella), anterior superior iliac spine.
Temperature: This is rarely tested. If pinprick is impaired, test
temperature sensation with a tuning fork (cold) and your hand (warm).
The lateral spinothalamic tract carries sharp pain and temperature.
The dorsal columns carry soft touch (most of it), deep pain (pinch
Achilles tendon) and joint position sense.
Dermatomes
Remember to perform Rombergs test: Ask the patient to stand with
his feet together and tell the patient you are ready to catch him if he
falls. If he stands with his eyes open and falls with his eyes closed,
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this is loss of joint position sense (Rombergs test is positive), as with

a posterior column lesion in the spinal cord or peripheral neuropathy.
If he is unable to stand with his eyes open and feet together, then this
is severe unsteadiness, most commonly due to cerebellar syndromes
and central and peripheral vestibular syndromes.
Figure 6.2: Dermatomes
In testing sensation, the candidate should show understanding of

the need to move from areas of reduced to normal sensation when
cutaneous sensitivity.
It is sensible to think whether the pattern fits a dermatomal
distribution or a peripheral neuropathy. If the sensory loss looks as if
it is in a glove and stocking distribution, start at the tips of the fingers
and toes, and work up until you find a sensory level.
Sensory abnormalities that suggest non-organic (functional) loss:
This is suggested by a non-anatomical distribution of sensory deficit
frequently with inconsistent findings.

Features which suggest a cortical basis for the sensory loss, e.g.
sensory suppression, asterognosis.
Disorders of Higher Cortical Function

Where appropriate, the candidate should be able to assess higher
cortical functions:
Memory (e.g. short term memory as in MMSE)
Orientation (in time and place)
Parietal lobe signs are agnosia, apraxia, and dyslexia.
This may be a particular elegant thing to do in view of a
demonstrated hemianopia.
Disorders of Gait
Candidates are expected to assess gait, if appropriate.
Gait abnormality may be exacerbated by asking the patient to heeltoe walk, walk on the toes or heels, or by asking the patient to walk
for a few steps with the eyes shut (sensory ataxia).
Specific disorders of gait referred to in the MRCP Clinical
Guidelines are:
Stamping gait (dorsal column loss)
Myopathic waddling gait
Hemiplegic gait/spastic/circumducting (cord paresis)
Paraplegic gait
Unilateral foot-drop gait
Bilateral foot-drop gait: S1 root lesion, CVA, peripheral neuritis
Parkinsonian gait
Broad-base gait: Cerebellar syndrome.
PROXIMAL MYOPATHY
This 45-year-old woman has weak legs. Please examine her legs and
elucidate why.
Causes of a proximal myopathy:
Inherited: Myotonic dystrophy, muscular dystrophy.
Endocrine: Cushings syndrome, hyperparathyroidism,
thyrotoxicosis, diabetic amyotrophy.
Inflammatory: Polymyositis, rheumatoid arthritis,dermatomyositis.
Metabolic: Osteomalacia.
Polymyalgia rheumatica.
Periodic paralysis due to channelopathies.
163
Malignancy: Carcinoma, paraneoplastic, Lambert-Eaton

myaesthenic syndrome.
Drugs: Alcohol, steroids.
Uraemia.
Investigations: EMG no denervation, repetitive discharges; CK; muscle
biopsy; ESR, CRP; thyroid function tests; dexamethasone suppression
test; anti-AChR antibodies; CXR thymoma, lung malignancy.
HEMIPLEGIA
elucidate why.
Having elicited the signs in the limbs, test for sensory inattention,
visual inattention and hemianopia, and ask if you may test the patients
speech. Show that you are considering the aetiology by feeling the
patients pulse (atrial fibrillation), auscultation for valve lesions and
carotid bruits, and taking the patients blood pressure. There is a
sided upper motor neurone weakness of the facial muscles, with
increased tone and hyper-reflexia. The plantar is extensor, and
abdominal reflexes are diminished. The most likely causes are
cerebrovascular accident due to cerebral thrombosis, haemorrhage
or embolism; brain tumour. A right-sided hemiplegia associated with
dysphasia woulod suggest that the causative lesion is affecting the
speech centres in the dominant hemisphere as well as the motor cortex
(precentral gyrus) and if there are sensory signs the sensory cortex
(postcentral gyrus). If cerebrovascular in origin, the causative lesion
is likely to be in the carotid distribution.
PARKINSONISM/PARKINSONS DISEASE
This 55-year-old man has found himself with walking problems.
Examine his upper limbs and elucidate why.
An Extremely Common Causes

The three features are tremor, rigidity and bradykinesia. In latter
stages, postural instability is the fourth feature.
Causes of Parkinsonism: Idiopathic Parkinsons disease, Parkinson Plus
syndromes (Multiple system atrophy, progressive supranuclear palsy:
Steele-Richardson-Olsewski, cortical Lewy body disease), druginduced, particularly phenothiazines, anoxic brain damage from
anoxia, neurosyphilis, post-encephalitis, MPTP toxicity (frozen addict
syndrome).

Pathology: Degeneration of the dopaminergic neurones between the
substantia nigra and basal ganglia.
Monotonous tone/dysarthria/dysphonia.
Withdrawn facies (expressionless face with absence of spontaneous
movements); dribbling of saliva.
Supranuclear gaze palsy.
Asymmetrical resting tremor; tremor disappears on voluntary
movement.
This tremor is a coarse, pill-rolling tremor (4-6 cps) at rest is
characteristic.
Bradykinesia as demonstrated by thumb finger opposition/tapping
one hand with the other/tapping foot on the floor. Cogwheeling
rigidity marked with synkinesis.
Muscle rigidity throughout the range of movement (tremor =
cogwheeling).
Festinant gait. Watch the difficulty when turning. Check righting
reflexes by standing behind the patient and gently pushing them
forwards and pulling them backwards.
Stooped, flexed posture with loss of arm swing.
Speech is slow, faint and monotonous.
Facial expression
Eye movements
Micrographia and impaired dressing ability.
Glabellar tap sign (on repeated tapping of the glabella, the
Parkinsonian patient continues to blink).
Extra points: BP looking for evidence of multisystem atrophy
(Parkinsonism with postural hypotension, cerebellar and pyramidal
signs), vertical eye movements for progressive supranuclear palsy,
dementia and Parkinsonism (Lewy-body dementia), ask for a
medication history.
Diagnosis is made by clinical observation, a therapeutic trial of
levodopa, or an apomorphine challenge. Other tests include MRI
(abnormal hypointensity in the putamen of patients with multiple
system atrophy), copper and caeruloplasmin measurements, testing
of automonic function (including sphincter electromyography).
Treatment: Forge a therapeutic alliance between the patients, carer
and specialists, assess disability and cognition, antmuscarinic
medication where there is drug-induced parkinsonism, consider drugs
when the condition is interfering with life, dopamine agonists, e.g.
pergolide, ropinirole and pramipexone which are well tolerated.
165
Ropinirole carries a much lower risk of dyskinesia. Other medications

include MAO-B inhibitors, e.g. selegiline, inhibit the breakdown of
dopamine; anticholinergics are effective for reducing tremor,
particularly drug-induced; L-dopa with a peripheral dopadecarboxylase inhibitor, e.g. madopar (problems with nausea and
dyskinesia, effects wear off after a few years so generally delay
treatment as long as possible, end of dose effect and on/off motor
fluctuation may be reduced by modified release preparations).
Levo-dopa without a decarboxylase inhibitor cause nausea and
vomiting and postural hypertension so it is always combined with a
decarboxylase inhibitor. Side effects of Levo-Dopa include involuntary
movements, psychiatric disturbance, nightmares, hallucinations, frank
psychosis, fluctuations in response including on/off syndrome. COMT
inhibitors (e.g. entacapone) block breakdown of L-dopa outside the
brain thus reducing motor fluctuations.
Surgery: Thalamotomy, pallidotomy, deep brain stimulation (e.g.
pallidal) and fetal neural transplantation [this may be dependent on a
referral to a tertiary centre, if necessary.] The next step is the addition
of a COMT inhibitor; and apomorphine given as SC injection or
infusion.
Other issues: Symptomatic treatment may be necessary (constipation
with stool softeners, laxatives or enemas), bladder symptoms (look
for the presence of a UTI; detrusor hyperactivity can be treated with
oxybutinin), postural hypotension (a tilted bed or fludrocortisone).
Patients can drive with PD provided that they are not severely disabled
by their PD and do not have sleep attacks during driving (this may be
drug-induced). Sophisticated vehicle adaptation is possible with
joysticks and infrared controls.
Carers should be aware of the Crossroads scheme. The Parkinsons
Disease Society provides support for patients and carers.
UNILATERAL FOOT DROP

elucidate why.
Here the main differential diagnosis is between:
Pyramidal lesion affecting lower limb (e.g. cerebrovascular
accident, multiple sclerosis: Pyramidal weakness, hyperreflexia and
upgoing plantar should make the diagnosis obvious).
Common peroneal nerve palsy: Weakness of dorsiflexion of the
feet and toes and of eversion of foot. Ankle jerk is intact and plantar

response normal; the ankle reflex is conveyed through the S1 root
via the tibial branch of the sciatic nerve, and is therefore spared in
a peroneal nerve lesion. Sensory loss often restricted to the dorsum
of the foot (may extend to anterolateral aspect of the leg below
the knee), including the first phalanges of the toes and the
anterolateral aspect of the bottom half of the leg. Causes include
compression or trauma at the fibula neck, diabetes mellitus,
vasculitis, and leprosy (look also for thickening of peripheral nerves
which become palpable, notably the greater auricular nerve).
L5 lesion often due to prolapsed intervertebral disc. Weakness of
dorsiflexion but not eversion of the foot (latter supplied by S1).
Ankle jerk is intact, plantar response normal, sensory loss on
dorsum of the foot often extending to the lateral aspect of the leg
below the knee.
CEREBELLAR SYNDROME
This 46-year-old woman, with a previously treated breast lump, now
finds herself with some problems buttoning her shirt. Please examine
her cranial nerves and suggest why.

Causes: Posterior fossa syndrome, alcohol, demyelinating disease,
trauma, rare, inherited, e.g. Fredreichs ataxia (pes cavus,
kyphoscoliosis, spastic paraparesis with extensor plantars, but areflexia
due to an axonal neuropathy, spinocerebellar degeneration causes
ataxia, diabetes mellitus in 10% of patients, cardiomyopathy), antiepileptic medication, stroke, paraneoplastic cerebellar syndrome,
severe hypothyroidism, ataxia-telengectasia, lesions at the
cerebellopontine angle, congenital disorders such as a Dandy-Walker
syndrome or Arnold-Chiari malformation.
Cerebellar dysarthria (slurred speech): Scanning dysarthria.
Finger-nose (dysmetria, intention tremor) and heel-knee-shin tests;
dysdiadochokinesis in upper limbs.
Hypotonia/pendular knee jerk.
Overshooting phenomenon/rebound phenomenon.
Nystagmus. In a cerebellar lesion, the fast-phase direction is
towards the side of the lesion, and maximal on looking towards the
lesion. Check also for broken pursuit and slow saccadic movements.
Truncal ataxia characteristics from a vermal lesion (rather than
limb ataxia).
Cerebellar ataxia (gait abnormality).
167
Differential diagnosis: Wilsons disease, Refsums disease (pes cavus,

retinitis pigmentosa, nerve deafness, anosma, cerebellar ataxia;
autosomal dominant).
Investigations: MRI is better than CT in posterior fossa, LP if there is
no space occupying lesion, phenytoin level, blood alcohol, gGT, LFT,
thyroid function tests, HIV test, glucose, lipids. CXR lung cancer
causing paraneoplasic syndrome, or with multiple metastases. ECG.
Management: Is there anything to be repairedtumour aneurysm?
Ensure abstinence from alcohol. Give thyroxine replacement. Reduce
phenytoin dose.
SPASTIC PARAPARESIS
This 40-year-old man has weak legs. Please examine his legs and offer
some explanations to the examiner why.
Never forget to demonstrate a sensory level and for absence of
the abdominal reflexes. Tell the examiners that you would normally
ask the patient about bowel and bladder function and test sacral
sensation.
The hypertonia, clonus and hyperreflexia tell you that the lesion
lies above L1 as the pyramidal tracts end there. Lesions below L1 can
result in cauda equina compression. This too is a medical emergency:
Flaccid paraparesis, saddle anaesthesia, reduced reflexes, downgoing
plantars, sphincter disturbance.
History is crucial (trauma, malignancy, pain in the spine, onset).
Common Causes
Cerebral palsy (check for intellectual impairment, behavioural
problems, a history of birth injury),
Demyelination/multiple sclerosis (commonest),
Spinal cord compression (medical emergency, disc prolapse above
L1/L2, malignancy, trauma, fracture of the vertebra), cervical
myopathy,
Trauma,
Motor neuron disease (no sensory signs),
Transverse myelitis,
Anterior spinal artery thrombosis (dissociated sensory loss with
preservation of dorsal columns),

Syringomyelia with typical upper limb signs, subacute combined
degeneration of the spinal cord,
Hereditary spastic paraparesis,
Fredreichs ataxia,
Parasagittal falx meningioma,
Cervical spondylosis,
Infection (e.g. HIV, abscess, syphilis, Potts disease of the spine,
HTLV-1 (tropic spastic paraparesis),
Radiation myelopathy,
Vascular (arterial occlusion),
Other inflammatory causes (sarcoid, SLE),
Intrinsic cord pathology (vitamin B12 deficiency, AVM).
Clinical signs: Contractures, wheel-chair and walking sticks (disuse
atrophy and contractures may be present if chronic), urinary catheter
in-situ, bilateral symmetrical paralysis of the lower limbs, symmetrical
lower limb hyperreflexia, bilateral extensor plantar responses, ankle
clonus, wasting, sensory level to mid-thoracic region, scissoring gait.
L2/3 Hip flexion
L3/4 Knee extension
L4/5 Foot dorsiflexion
knee jerk L3/4
L5/S1 Knee flexion, hip extension
S1/2 Foot plantar-flexion
ankle jerk S1/2
The term level is a very indescript term, but literally means
sensory level, reflex, and motor level (both at the level), and tone
(below the level). Any sensory level must be determined, particularly
if the history suggests an acute or subacute onset with recent alteration
in sphincter function. See Fig. 7 for a pictorial representation of the
dermatomes.
Localisation of the level of the lesion can be achieved by:
Spasticity of the lower limb alone: Lesion of the thoracic cord (T2
L1)
Irregular spasticity of the lower limbs with flaccid weakness of
scattered muscles of lower limbs: Lesion of lumbosacral
enlargement (L2 S2).
Examine for a sensory level suggestive of a spinal lesion. Look at
the back for scars or spinal deformity. Search for features of multiple
sclerosis, e.g. cerebellar signs especially dysarthria, fundoscopy to
look for optic atrophy. Ask about bladder symptoms and note the
presence or absence of urinary catheter. State that a complete
examination would include anal tone.
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Figure 6.3: Dermatomes of lower limb
If allowed to proceed, you should examine the arms. You may be

able to localise the lesion. Ask the examiners permission to test the
neck movements.
Investigations: Suspicion of spinal cord compression is a medical
emergency. Once sphincter dysfunction has been present for 24 hours,
it is irreversible. Therefore, the necessary investigations must be
carried out as a matter of urgencyFBC, ESR, CXR, plain radiology of
the spine, then either a CT myelogram or MRI. A neurosurgeon should
be contacted. Depending on the likely differential diagnosis:
Electromyography, nerve conduction studies, lumbar puncture (CSF
for oligoclonal bands, culture, acid-fast bacilli, ACE), blood and CSF
syphilis, blood culture, biopsy of masses, HIV test, vitamin B12 levels,
CRP, autoantibodies and MRI of the central nervous system.
Management: This is dependent on the cause. Spinal cord compression
with bladder or bowel involvement often requires surgical
decompression. Stabilisation of the spine may be necessary.
Dexamethasone and radiotherapy may suffice for malignant
compression. The problem with benign tumours is that the paraparesis
may be attributed to multiple sclerosis, despite the symptoms not
being disseminated in time and place. With malignancy, the main
danger is indecision; the condition is obviously incurable but surgical
treatment at an early stage may relieve pain, minimise weakness and
preserve bladder function.
Common Neurological Cases

of a diagnosis or differential diagnoses. Common neurological cases
SPEECH DISORDERS
The physiology of speech consists of three distinct aspects; phonation
(generation of noise through the vocal cords), articulation (of the noise
into comprehensible sounds) and language and understanding
(fluency, comprehension, word formation, etc.). Therefore,
abnormalities in either of these processes (dysphonia, dysarthria and
dysphasia) may yield a speech abnormality, and when faced with a
case in the exam, though the latter aspect is the most likely to require
assessment, you must be able to assess speech in its entirety.
Dysphoniacan the patient generate the effort to push air through
the vocal cords (myasthenia and other neuromuscular conditions
normal at first but starts to fade), or is there an obstruction within
the larynx or the recurrent laryngeal nerve impeding adequate
phonation.
Dysarthriaare the words fluent or stuttery? Can the patient
pronounce vowels correctly EE or AA other useful ones are P
and B. Are there gross articulation problems when coordination of
speech is tested British constitution (cerebellar). Does the articulation
sound mumbling (Parkinsons also dysphonia). Assessment of
dysarthria:
1. Monotonous speech of Parkinsonism.
2. Staccato or broken speech of cerebellar syndrome.
3. Hot potato speech of pseudobulbar palsy: Usually bilateral
pyramidal signs, spastic tongue, brisk jaw jerks.
4. Nasal speech of bulbar palsy: Flaccid and often fasciculating
tongue, and other signs of MND.
5. Dysarthria (unclassified) usually following stroke with incomplete
recovery.
Examine the motor system: LMN weakness (facial palsy, bulbar palsy),
UMN weakness (hemiparesis, pseudobulbar palsy), cerebellar disease
nystagmus, intention tremor, hypotonia and ataxia, extrapyramidal
disease (Parkinsons disease).
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Dysphasia: This should be assessed in terms of object naming (nominal),

fluency and repetition (expressive) and comprehension, e.g. by asking
the patient to perform simple commands (receptive). Repetition can
be performed by difficult words, e.g. statistican analysis, No ifs ands
or buts. Finally, remember that dysphasic speech problems usually
imply a lesion in the left dominant frontotemporal region, and other
complimentary signs should be sought (right hemiparesis). The
presence of a dysphasia will also suggest a cortical lesion when faced
with a patient that looks like a stroke, rather than a lacunar syndrome
(internal capsule). Test the patients inability to name objects (wrist
watch, second hand and winder on watch). Difficulty in naming objects
is found in both motor and sensory aphasia but is relatively selectively
impaired in the rare nominated dysphasia (lesion on angular gyrus).
You may be asked the site of the lesion:
Brocas area: Inferior frontal gyrus of the dominant hemisphere.
This produces non-fluent aphasia. The content may be good, but
the patient says little.
Wernickes area: Posterior part of superior temporal gyrus plus
adjacent parts of parietal and occipital cortex of dominant
hemisphere.
MOVEMENT DISORDERS
Resting tremor: Parkinsons disease.
Postural tremor (worse with arms outstretched): Benign essential tremor,
anxiety, thyrotoxicosis, metabolic: carbon dioxide and hepatic
encephalopathy, alcohol. Look for the signs of thyroid disease, and
tell the examiner you would like to know if there is any family history
of tremor, and if the patient is on any medications (e.g. salbutamol,
lithium).
Intention tremor: Seen in cerebellar disease. Look for other cerebellar
signs.
Dystonic posturing: Co-contraction of agonist and antagonist which
may lead to an intermittent or persistent maintainence of abnormal
pasture.
Chorea: Non-rhythmic movements of a rapid, jerky nature which
frequently appear pseudo-purposeful.
Athetosis: Slower writhing, irregular movements predominantly in the
hands and wrist.

Others (in cranial nerve territory): Hemifacial spasm
Myokymia
Blepharospasm
Orofacial dyskinesia.
MULTIPLE SCLEROSIS
This 30-year-old woman complains of double vision and
incoordination with previous episodes of weakness. Please perform a
neurological examination of her legs and suggest a likely diagnosis.

Key signs: Optic neuritis (you may not be allowed to examine the eyes
but you may ask May I ask about eye problems), internuclear
ophthalmoplegia (frequently bilateral in MS), reduced visual acuity,
and other cranial nerve palsy. In an internuclear ophthalmoplegia, on
looking to the right, the right eye abducts normally but the left eye is
unable to adduct; the right eye has nystagmus.
Peripheral nervous system: Upper motor neuron spasticity, weakness,
brisk reflexes, altered sensation.
Sensory alteration: Often hot/cold appreciation is disturbed, or there
is a history of Lhermittes phenomenonelectric shock like pain on
flexing the neck which shoots down the arms and legs and is caused
by disease abutting the dorsal columns.
Higher cortical function: Euphoria, depression and disinhibition.
Autonomic: Urinary retention/incontinence, impotence and bowel
problems.
Signs of disseminated lesions in CNS.
Investigations: MRI is most useful to detect involvement and
characteristic pattern of lesions, lumbar puncture is now less regularly
used.
Visual evoked response is useful in a patient with an isolated lesion
which may be due to multiple sclerosis to identify subclinical
involvement and provide evidence for demyelination (SSEPs are used
as well).
CSF shows an increase in total protein, and oligoclonal bands (not
matched in serum).
Central nervous system demyelination causes neurological
impairment that is disseminated in both time and space.
Benign course more likely if there is pure sensory presentation,
infrequent relapses and long remissions, onset with optic neuritis or
sensory or motor symptoms, or benign condition 5 years after onset.
173
Complications: Visual loss, paresis, tremor and incontinence; significant

cognitive impairment may occur late.
Management: Supportive, including catheters, etc. as appropriate,
methylprednisolone, be prepared to discuss interferon. CSF:
Monoclonal IgG bands, MRI: Periventricular white matter plaques,
visual evoked potentials: delayed velocity but normal amplitude (often
even where there is no evidence of optic neuritis, indicating that there
is some neuronal loss sustained). Diagnosis can be made clinically
(e.g. 2 or more attack with 2 or more objective clinical lesions), or a
combination of clinical and corroborative data (e.g. 2 or more attacks
+ 1 objective lesion + MRI / +ve CSF).
Treatment: Multidisciplinary team (nurse, physiotherapist, occupational
therapist, social worker, and physician); disease-modifying treatments
(-interferon) and symptomatic treatments (methylprednisolone
during the acute phase may shorten the duration of the attack but
does not affect propnosis), anti-spasmodics, e.g. tizanidine,
clonazepam, dantrolene, baclofen, carbamazepine (for neuropathic
pain), cognitive and emotional problems (emotionalism, depression
using anti-depressant medication or psychological treatments such as
cognitive behavioural therapy, anxiety), speech difficulties (specialist
speech and language therapist), sexual dysfunction, laxatives and
intermittent catheterisation/oxybutinin for bowel and bladder
disturbance. Consider the impairment, disability and handicap: Arm
paralysis is the impairment, inability to write is the disability,
subsequent inability to work in a job is the handicap. Occupational
therapy for rehabilitation.
The key points are outlined in the National clinical guideline for
diagnosis and management of multiple sclerosis in primary and
secondary care (The Royal College of Physicians, The Chartered
Society of Physiotherapy).
DIABETIC AND PERIPHERAL NEUROPATHY

This patient has noticed generalised weakness/tingling of his fingers.
Please examine the motor and sensory system in the upper limbs to
establish the cause.

This is done quickest by assessing vibration loss with the vibrating
tuning fork applied to the bony prominence of the metatarsal head,
malleoli, patella and if required anterior superior iliac spine.

If you cannot detect a peripheral neuropathy, then you must resort
to performing an orthodox sensory examination as prescribed.
Ensure that, if given the time, you perform sufficient tests to
determine function in the two main sensory tracts (this usually
means pinprick and vibration testing).
If during the course of your sensory assessment, there is a gross
sensory loss that is bilaterally symmetric then proceed to
determine if a sensory level exists. Motor loss may be present in
mixed motor/sensory neuropathies.
Sensory loss: Look for foot ulcers, roughened thickened callous skin,
tropic changes and Charcot joints (common causes of these: diabetes
mellitus and syringomyelia).
Palpate for tenderness of affected muscles which is common in
diabetic or alcoholic polyneuropathy. Palpate for thickened
peripheral nerves present in: Refsums disease (cerebellar damage,
peripheral neuropathy, deafness and retinitis pigmentosa),
Amyloidosis, Leprosy, Dejerine-Sottas disease, Charcot-MarieTooth disease some thickening detectable in 25% of cases.
Glance briefly for clues as to the cause: Insulin injection sites (diabetes
mellitus), signs of chronic liver disease (especially alcoholic),
anaemia and slight jaundice (B12 deficiency), cachexia (malignancy),
pigmentation, anaemia and brown line on nails + evidence of
haemodialysis (uraemia), pes cavus (HSMN or Fredreichs ataxia),
rheumatoid hands or butterfly rash of systemic lupus
erythematosus.
Sphincter function: You should enquire about bladder and bowel
function by asking the examiner. Along with the obvious catheter
tube, sphincter disturbances should be suspected in patients with
impaired saddle region anaesthesia.
Enquire about vision: Causes according to sensory/motor:
Predominantly sensory (carcinomatous neuropathy, diabetes
mellitus, uraemia, alcohol, drugs, e.g. isoniazid and vincristine,
vitamin deficiency, e.g. B12 and B1); predominantly motor (GuillainBarr syndrome and botulism acutely, lead toxicity, porphyria,
HSMN). The broad areas of aetiology are acute symmetrical
peripheral neuropathy, multiple neuropathy, and chronic
symmetrical peripheral neuropathy.
Broad Classes of Causes

Mononeuritis multiplex: Diabetes mellitus, connective tissue disease,
e.g. SLE and rheumatoid arthritis, vasculitis, e.g. polyarteritis
nodosa and Churg-Strauss syndrome,
175
Infection, e.g. HIV, malignancy. Hereditary: E.g. HMSN-1 and -2

Inherited disorders: Refsums disease, Fredreichs ataxia.
Drug causes: Isoniazid, nitrofurantoin, phenytoin, ciclosporin,
vincristine, amiodarone, cisplatin.
Deficiencies: Vitamin B 12, folate, thiamine (Wernickes
encephalopathy and Korsakoffs psychosis in alcohols) and niacin
(pellagra).
Collagen vascular disease: E.g. SLE, rheumatoid arthritis, polyarteritis
nodosa, scleroderma.
Malignant disease.
Malignancy.
Endocrine, e.g. diabetes mellitus, uraemia, hypothyroidism
Others, e.g. porphyria and amyloidosis.
Idiopathic.
Causes of a predominantly motor neuropathy: Carcinomatous
neuropathy, lead, porphyria, Charcot-Marie-Tooth.
Investigations: Urine for glucose and protein, haematology (ESR,
vitamin B12 level, folate, FBC), biochemistry (fasting blood glucose,
renal function, liver function, TSH), neurophysiological tests,
immunology (ANA, ENA, ANCA), chest X-ray, urine (Bence-Jones
protein), CSF, immunology (anti-neuronal antibodies, anti-HIV), tests
for Sjogrens syndrome, molecular genetics test, nerve conduction
studies (diagnosis confirmed by slowing of motor or sensory
conduction velocities, moderate in axonal type and marked in
demyelinating type), CSF (in GBS/inflammatory neuropathies for
raised protein level), nerve biopsy in progressive neuropathy or to
identify vasculitis as the cause (sensory nerves are usually biopsied),
imaging (screening for malignancy in patients with suspected
paraneoplastic neuropathy; skeletal survey for myeloma; chest
radiography for suspected sarcoidosis), DNA analysis (for hereditary
sensorimotor neuropathies); bone marrow biopsy (for vitamin B12
deficiency or myeloma). Management: Tight control of diabetes,
consider other related problems in eye and kidney, educate patient
about the need to control foot inspection, etc.
Management: Directed towards the specific cause. Rigorous control of
glycaemia, often with intensive insulin regimens, can improve diabetic
neuropathy, particularly if the syndrome arose acutely. Simple
analgesics, tricyclic anti-depressants, anticonvulsants (phenytoin and
carbamazepine) may help. Autonomic neuropathy is difficult (postural
hypotension: Fludrocortisone; vomiting: metoclopramide; bacterial

overgrowth: Erythromycin). In deficiency, vitamin B12 for subacute
combined degeneration of the cord.
ULNAR NERVE PALSY

This 72-year-old lady with worsening osteoarthritis has difficulty using
her hands. Please examine her upper limbs from a neurological
perspective, and suggest why.
Usually due to lesion at the elbow; inspect for scars or arthritis.
The hand shows generalized muscle wasting and weakness which
spares the thenar eminence. There is sensory loss over the fifth finger,
the adjacent half of the fourth finger and the dorsal and palmar aspects
of the medial aspect of the hand.
In a low ulnar nerve lesion, the hand is claw shaped the
metacarpophalangeal (MCP) joints of the ring and little fingers are
hyperextended and the interphalangeal joints remain flexed. There is
weakness in abduction and adduction of the fingers and thumb.
Sensation is impaired over the medial sign of the hand, little finger
and medial (ulnar) border of the ring finger. In a high lesion, the
FDPs are also paralysed. The DIPs are not flexed, and so the clawing
is less obvious. This is termed the ulnar paradox. Low lesions occur
at the wrist, but high lesions occur in osteoarthritis and dislocations,
commonly at the elbow.
Occasionally due to repeated trauma to heel of hand (no sensory
loss in this case). Common causes are fracture or dislocation at the
elbow, and osteoarthrosis at the elbow with osteophytic encroachment
on the ulnar nerve in the cubital tunnel. Other causes are occupations
with constant leaning on elbows (secretaries), excessive carrying angle
at the elbow, injurie at the wrist or palm (e.g. occupations using
screwdrivers, drills, etc.)
MEDIAN NERVE PALSY

This 72-year-old lady with worsening rheumatoid arthritis has
difficulty using her hands. Please examine her upper limbs from a
neurological perspective, and suggest why.
Carpal tunnel syndrome is a common case.
NB. Associations include pregnancy, myxoedema, rheumatoid
arthritis, acromegaly, trauma. Remember that sensory loss is very
variable since the palmar branch of the median nerve passes superficial
to the flexor retinaculum.
(Please note that this would make a suitable case for Station 5 as
well).
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RADIAL NERVE LESION

This 30-year-old with a remitting alcohol dependence syndrome was
referred from casualty because of problems with his hands. Please
examine his upper limbs neurologically, and discuss with the examiners
the possible diagnosis.
The commonest cause of this rare condition is Saturday night palsy
where the nerve is compressed against the middle 1/3 of the humerus
and brachioradialis and supinator are also paralysed as well as the
forearm muscles.
There is wrist drop and the patient is unable to straighten their
fingers. There is sensory impairment over the 1st dorsal interosseus.
Straightening of the fingers at the IP joints is made possible if the
wrist is passively straightened because the intrinsic muscles of the
hand supplied by the ulnar nerve (interossei and lumbricals) permit
some extension. No extension is possible at the MCPs. Grip strength
is impaired in a radial nerve lesion, not because any of the flexors are
weak but because a degree of wrist extension facilitates good grip.
Likewise, abduction and adduction of the fingers are both unaffected
in a radial nerve palsy but may appear to be with a flexed wrist.
Check elbow extension and check the triceps reflex. An intact triceps
reflex indicates a lesion below the spinal groove. Triceps wasting and
an absent reflex implies a high axillary radial nerve lesion or a C7
radiculopathy. C7 lesion causes weakness of shoulder adduction,
elbow extension, wrist flexion and wrist extension, because it makes
a significant contribution to both median and radial nerves. A radial
nerve lesion cannot affect shoulder adduction or wrist flexion.
Management: The prognosis is good; in compression, recovery is over
weeks. Even if the wrist requires splinting, muscle function starts to
recover 4-8 months later. The wrist must be splinted in extension as
must the MCP joints the latter not rigidly.
CEREBROVASCULAR ACCIDENT / STROKE

Examine this patients upper limbs neurologically and then proceed
to examine anything else that you feel is important if time before
discussing your findings with the examiners within the time allowed.

Symptoms: The duration of onset is crucial for the differential diagnosis.
An abrupt onset of neurological deficit with a tendency to improve,

with or without preceding transient ischaemia, in the presence of
cardiovascular risk factors. A protracted illness with a slowly
worsening circadian headache, drowsiness, vomiting, symptoms
attributable to focal brain damage and seizures suggest a spaceoccupying lesion. The nature of the lesion usually dictates the speed
of onset, e.g. meningioma or breast cancer metastases.
Definition of stroke: Rapid onset, focal neurological deficit due to a
vascular lesion > 24 hr.
Key signs: Vary dependent on stroke.
Inspection: Walking aides, nasogastric tube or PEG tube, posture (flexed
limbs and extended lower limbs), wasted or oedematous on the
affected side. Asymmetrical facial droop.
Pyramidal posture: The upper limb tends to be flexed at the elbow,
pronated and internally rotated and internally rotated at the shoulder,
and the lower limb extended at the hip and knee, with the foot inverted
and plantar-flexed.
Pyramidal drift: Perhaps the only sign.
Weakness in the motor divisions of the cranial nerves +
homonymous quadrantanopia/hemianopia; there may be
papilloedema. Check for gag reflex.
Dysphasia: Brocas area anterior lesions causing an expressive
dysphasia with non-fluent speech but intact understanding; the patient
should be asked to write; Wernickes area posterior lesions causing
a receptive dysphasia can be difficult to identify; the speech is fluent
but mistakes made in syllables to talking fluent nonsense can occur.
Tone: Spastic rigidity, clasp-knife (resistance to movement, and
then sudden release). Ankles may demonstrate clonus (>4 beats).
Power: Hemiparesis.
Reflexes: Asymmetrical hyperreflexia.
Unilateral extensor plantar response.
Coordination: Reduced, often due to weakness (but can be seen in
posterior circulation strokes)
Characteristic gait and paucity of movement.
Extra Points
Upper motor neuron unilateral facial weakness (spares frontalis due
to its dual innervation).
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Gag reflex and swallow to minimize aspiration.

Visual fields and higher cortical functions, e.g. neglect helps
determine a Bamford classification.
Cause: Irregular pulse (AF), blood pressure, cardiac murmurs or carotid
bruits (anterior circulation stroke).
Aetiology
Ischaemic stroke (cardiovascular disease and risk factors,
prothrombotic tendencies, vasculitis, internal carotid dissection, foci
for emboli), haemorrhage (hypertension, aneurysm, e.g. SAH, AVM,
thrombocytopaenia or bleeding diatheses). Differential diagnosis of a
hemiparesis: Space-occupying lesion (tumour, aneurysm, abscess,
haematoma, granuloma, tuberculoma, toxoplasmosis, cysts).
Anatomical Territory
Anterior cerebral artery (ACA) syndrome causes contralateral leg
weakness and sensory loss. Voluntary loss of micturition may be lost.
Middle cerebral artery syndrome may be indistinguishable from
internal carotid artery occlusion, leading to contralateral hemiparesis
(weak arm, face and often leg), contralateral hemisensory loss,
contralateral homonymous hemianopia, global dysphasia (if dominant
cortex), and severe agnosias and apraxias. Posterior circulation strokes
cause bilateral weakness or sensory loss, cerebellar signs, e.g. ataxic
hemiparesis and diplopia.
Investigations
CT new guidelines suggest within 24 hours. As 80-90% of strokes
are ischaemic, a CT scan is not always necessary. However, it is
definitely indicated if there is any suggestion of an intracranial
haemorrhage or doubt about the aetiology. In practice, most patients
have a CT scan. If there is swelling of cerebellar or brainstem disease,
a CT scan is necessary as swelling in the posterior fossa can be rapidly
life-threatening. CT + contrast will identify a mass lesion.
Bloods: FBC, ESR (young CVA may due to arteritis), glucose, renal
function.
Blood cultures if suspicion of infective endocarditis.
Do consider carotid and cardiac investigations I would like to
know if the patient has ever had an irregular pulse or chest pain.
ECG: AF or previous infarction.

CXR: Cardiomegaly or aspiration.
Echocardiogram.
Carotid Doppler ultrasound.
MRI/MR angiography.
Tests looking for risk factors such as cholesterol, Hb for
polycythaemia, diabetes. Thrombophilia screen (protein C and S,
antithrombin III, factor V Leiden). ANA, dsDNA, C3, C4.
Bamford classification of stroke (Lancet, 1991).
Total anterior circulation of stroke (TACS): Motor or sensory deficit
(contralateral to the lesion), homonymous hemianopia
(contralateral to the lesion), higher cortical dysfunction, e.g.
dyspasia, dyspraxia and neglect.
Partial anterior circulation (PACS) 2/3 of the above.
Lacunar (LACS): Pure hemi-motor or sensory loss.
Posterior circulation stroke (POCS): Isolated hemianopia, brainstem
signs, cerebellar ataxia.
Dominant parietal lobe cortical signs: Dysphasia: Receptive, expressive
or global; Gerstmanns syndrome (dysgraphia, dyslexia or
dyscalculia), L-R disorientation, finger agnosia.
Non-dominant parietal-lobe signs: Dressing and constructional apraxia,
spatial neglect.
Management
Readers are advised to familiarize themselves with the current
National Guidelines for Stroke (from the Royal College of Physicians
of London), prepared by the Intercollegiate Stroke Working Party.
There is no single effective treatment for established stroke.
However, patient management should include looking for
reversible causes that may mimic stroke such as hypoglycaemia or
over anticoagulation and ensuring patient safety with regard to
the swallow reflex. Nursing in the unconscious position, assessing
skin condition and ensuring an adequate fluid intake. The family
should be interviewed early on and informed of the prognosis.
Brain imaging should be undertaken as soon as possible, at least
within 24 hours of onset. It should be undertaken as a matter of
urgency if the patient has been having anticoagulant treatment, a
known bleeding tendency, a depressed level of consciousness,
unexplained progressive or fluctuating symptoms, papilloedema,
neck stiffness or fever, severe headache at onset, or indications
for thrombolysis or early anticoagulation. If the result of a CT
scan is uncertain, MRI should be considered.
181
Blood pressure should be recorded but patients with high blood

pressure should not have this lowered in acute stroke as it may
result in an extension of the condition.
Complications such as pressure sores, aspiration, pneumonia,
contractures, deep venous thrombosis should be prevented.
Depression which is common in stroke patients and may occur in
up to 40% of these patients should be screened for and treated as
appropriate.
Mobilisation should occur as early as possible and this is best
achieved with a team approach directed by the physiothe rapist
with instructions to nurses to carry this on in the ward. The
occupational therapist is essential in the assessment and therapy
of simple procedures such as dressing, feeding and cooking.
Aspirin is indicated for any patient who suffers a transient ischaemic
attack and as secondary prophylaxis after cerebral infarction unless
there is a contraindication. Ideally, aspirin should be started within
48 hours. Anticoagulation is useful in patients under 80 who are in
atrial fibrillation or any patient who has a clear source of cardiac
emboli. Where treatment with warfarin is considered then cerebral
haemorrhage must be excluded by a CT scan. Some patients will
die as a result of their stroke and it is the responsibility of all
members of staff to ensure a comfortable and dignified death. It is
indicated for patients with atrial fibrillation, or ischaemic stroke
associated with mitral valve disease, a prosthetic valve or within 3
months of a myocardial infarction.
Intracranial haemorrhage requires an urgent neurosurgical opinion.
Referral to a specialist stroke unit: Multidisciplinary approach
(physiotherapy, occupational therapy, speech and language therapy
and specialist stroke rehabilitation nurses). This team should ideally
meet at least once a week.
Consider statins, carotid endarterectomy if carotid stenosis > 70%,
meticulous glycaemic control, low cholesterol diet, and physical
exercise. A reduction in risk of recurrent CVA has been
demonstrated for both hypertensive and normotensive patients
using perindopril (the PROGRESS study).
Acute Stroke/TIA
[Please note that, in 2007, guidelines were published in the UK by the
Royal Colleges of Physicians and NICE for an acute stroke.]
The NICE guideline covers the acute stage of a stroke or TIA,
mainly the first 48 hours after symptoms start. TIA is defined as stroke

symptoms and signs that resolve within 24 hours. There is evidence
for stroke that rapid diagnosis, admission to a specialist stroke unit,
immediate brain imaging and use of thrombolysis where indicated
can all contribute to a much better outcome for patients. For people
who have had a TIA, rapid assessment for risk of subsequent stroke
allows appropriate treatment to be started quickly to reduce the chance
of having another stroke.
Their key recommendations are that:
All patients with suspected stroke should be tested with the FAST
(Face Arm Speech Test) or similar test to recognize symptoms of
acute stroke.
All patients with acute stroke should be taken to hospital as quickly
as possible and transferred from A&E to an acute stroke unit.
Immediate CT scanning should be available 24/7 for those who
need it.
High risk patients who have already had a TIA should receive a
diagnosis, investigations and initial treatment within 24 hours.
All patients should receive a swallowing assessment within 24 hours
of assessment and before being given any oral food, fluid or
medication.
[The quick reference guide, patient versions of the NICE guideline
and the full NICE guideline at www.nice.org.uk/CG68].
MOTOR NEURON DISEASE

This patient was referred by the GP to a local hospital because he had
appeared to have lost weight. Examine his upper limbs, and offer
possible diagnosis.
MND is a progressive disease of unknown aetiology. There is axonal
degeneration of upper and lower motor neurons. Motor neuron
disease may be classified into three types: Amyotrophic lateral sclerosis
(50%) affecting the corticospinal tracts affecting predominantly
producing spastic paraparesis or tetraparesis, progressive muscular
atrophy (25%) affecting anterior horn cells predominantly producing
wasting, fasciculation and weakness (best prognosis), and progressive
bulbar palsy (25%) affecting lower cranial nerves and suprabulbar
nuclei producing speech and swallowing problems (worst prognosis).
Symptoms: Bulbardysarthria and dysphonia, dysphagia and difficulty
in chewing with nasal regurgitation of fluids, recurrent chest infections
and dyspnoea; limbsweakness of a hand or the whole upper limb,
with wasting that the patient has noticed, progressive foot drop;
183
cramps or fasciculations are common and can precede other symptoms

by months.
Dysarthria (pseudobulbar palsy: hot potato speech; bulbar:
Donald Duck speech due to palatal weakness), dysphonia,
Wheel-chair/stick,
Tongue: Wasting and fasciculation (bulbar) or a stiff spastic tongue
with brisk jaw jerk (pseudobulbar),
General fasciculations,
Wasting,
Tone: Usually spastic but can be flaccid,
Mixed upper and lower motor neurone signs (spasticity with
areflexia or flaccidity with hyperreflexia),
Reflexes: Absent and/or brisk,
No sensory deficits. No extra-ocular muscle, cerebellar or extrapyramidal involvement,
Sphincter and cognitive state disturbance is rarely seen,
Tell the examiner about your wish to enquire about possible
difficulties in swallowing.
Differential diagnosis: MSno sensory abnormality in MND,
polyneuropathies, cervical myelopathy, motor neuropathy, cord or
cauda-equina compression (causes sphincter disturbance which does
not occur in MND), myasthenia gravis (weakness of the external ocular
muscles does not occur in MND), diabetic amyotrophy, cervical and
lumbar stenosis. A key differential diagnosis in a tertiary unit is
progressive multifocal neuropathy.
Investigations: Clinical diagnosis, laboratory results are usually normal,
EMG fasciculation/denervation, fibrillation potentials and positive
sharp waves, abnormal motor units of increased amplitude and
potential, reflecting widespread anterior horn cell damage, NCS
usually normal, MRI excludes the main differential diagnosis of
cervical cord compression and myelopathy.
Management: Supportive, e.g. PEG feeding and NIPPV,
multidisciplinary approach to care, riluzole (glutamate antagonist)
slows disease progression by an average of 3 months but does not
improve function or quality of life and is costly. This has been
recommended by NICE for asymptomatic patients with amyotrophic
lateral sclerosis; it extends the time to mechanical ventilation in this
invariably fatal disease. Quinine is used for cramps. Baclofen,
dantrolene and diazepam are used for spasticity. Lactulose and

isphagula husk are used for constipation. Important nonpharmacological therapy includes counselling for depression,
radiotherapy to the parotid glands for excess saliva, and assisted
ventilation for respiratory failure.
OLD POLIO
This man is normally wheelchair bound.
Examine his lower limbs and suggest to the examiners why.
One of the legs is short, wasted, weak and flaccid with reduced
reflexes and a normal plantar response. There is no sensory defect.
The disparity in the length of the limbs suggest growth impairment
in the affected limb since early childhood. The complete absence of
sensory and pyramidal signs point to a condition affecting only lower
motor neurones. The diagnosis is old polio. Differential diagnosis
includes spinal muscular atrophy, AIDP and causes of a motor
neuropathy.
Examiners if pushy may ask you about post-polio syndrome.
HEREDITARY SENSORIMOTOR NEUROPATHY / CHARCOTMARIE-TOOTH DISEASE OR PERONEAL MUSCLE ATROPHY

This gentleman complains his legs begun to look unusual over the last
few years. Please examine his lower limbs neurologically.

Clinical Signs
Type I: Is a severe, symmetrical wasting of distal lower limb muscles
with preservation of the thigh muscle bulk (inverted champagne bottle
appearance), kyphoscoliosis, pes cavus (seen also in Fredreichs ataxia),
weakness of ankle dorsiflexion and toe extension, variable degree of
stocking distribution sensory loss (usually mild), gait is high-stepping
due to foot drop and stamping (absent proprioception), tremor in
upper limbs, wasting of small muscles of the hand, palpable lateral
popliteal nerve in some families only.
Presents in 1st decade with difficulty in walking, or foot deformity.
Type II: Tends to be confined to the lower limbs, wasting and
weakness is less severe, reflexes are absent in the lower limbs but
normal in the upper limbs, foot and spinal deformity are less common,
peripheral nerves are not palpable.
Later onset, with a peak in the second decade, but many cses
present in the middle or even late adult life, with weakness or wasting.
185
Differential diagnosis: Peripheral neuropathy, mononeuropathy, L4/5

root lesion (may cause bilateral foot drop but inversion at the ankle is
obviously lost, with dermatomal sensory signs), cauda equina lesions
(this must be actively considered where there are distal signs, e.g.
absent ankle jerk, and there is saddle anaesthesia and sphincter
involvement), and motor neurone disease (complete absence of sensory
involvement).
Discussion: Types I and II are distinct. Men are more severely affected
than women. The commonest HSMN types are I (demyelinating) and
II (axonal), autosomal dominant inheritance. The degeneration is
mainly in the motor nerves. It is sometimes also found in the dorsal
roots and dorsal columns, and slight pyramidal tract degeneration is
often seen. The condition usually becomes arrested in mid-life. Nerve
conduction velocity is severely reduced in type I, but is either normal
or slightly reduced in type II. Sural nerve biopsy demonstrates
hypertrophic onion bulb changes and reduced density of myelinated
fibres in type I. The reduction in conduction velocity indicates a severe
demyelinated neuropathy. Orthotic appliances and sometimes surgical
correction of the foot deformity or tendon transfer can affect affected
individuals. Type I is most usually dominantly inherited, but sexlinked recessive forms are also encountered. Mutations in PMP22
underlie commonly type I; myelin protein Po gene mutations have
been found in HSMN I and II.
FREDREICHS ATAXIA
This person has noticed unsteadiness for as long as he can remember.
Please examine his upper limbs, and anything else that you feel is
appropriate.
Clinical signs: Young adult, wheelchair, pes cavus, bilateral cerebellar
ataxia (ataxic handshake), pyramidal leg weakness (bilateral extensor
plantars), peripheral neuropathy with muscle wasting and loss of ankle
and knee jerks, posterior column signs (loss of vibration and joint
position sense), cerebellar signs in the arms, nystagmus and scanning
dysarthria, kyphoscoliosis, optic atrophy (30%), sensorineural deafness
(10%), listen for the murmur of HOCM, ask to dip the urine (10%
develop diabetes).
The oldest person to have presented to the National Hospital of
Neurology in London was in his early 60s but that is unusual.
Inheritance is usually autosomal recessive, onset is during teenage
years, survival rarely exceeds 20 years from diagnosis, there is an

association with HOCM, mild skeletal abnormality and mild dementia.
It is caused by an increased number of GAA trinucleotide repeat
sequences at a gene encoding the protein frataxin on chromosome 9.
MYOTONIC DYSTROPHY (DYSTROPHIA MYOTONICA)

This man complains of weakness in his hands. Please examine his
upper limbs.

Males > females, autosomal dominant, presentation in 3rd/4th decades
Symptoms: Myotonia is rarely intrusive initially, but the failure to release
grip can be troublesome. Myotonia is often worse when cold or excited.
Poor vision, weight loss, impotence, ptosis and increased sweating
are common. Later in the course of the disease, low-output cardiac
failure and hypersomnolence occurs. Stokes-Adams attacks can occur.
Clinical Signs
Myopathic facies (long, thin, expressionless),
Wasting of facial muscles (temporalis, masseter and
sternocleidomastoids),
Gynaecomastia,
Altered oesophageal and bowel motility,
Testicular atrophy,
Slow release of hand grip,
Percussion myotonia,
Generalised wasting and weakness of upper limbs (distal wasting
is more prominent in DM-1, proximal wasting is more prominent
in DM-2),
Bilateral ptosis,
Frontal balding (try to avoid this term when presenting in front of
the patient),
Cataracts,
Myotonia (difficulty in releasing grip on handshake),
Dysarthria due to myotonia of the tongue and pharynx,
Hyporeflexia and subsequently areflexia develop in later stages of
the disease due to muscle weakness and/or diabetic-related
peripheral neuropathy,
External ophthalmoplegia (rare),
Pacemaker,
187
Cor pulmonale due to diaphragmatic weakness with subsequent

hypoxaemia or heart failure,
Testes are small and firm.
The tingling in this case may be due to a neuropathy secondary
diabetes or muscle wasting from the disease itself.
Hands Grip my hand, now let go, Screw up your eyes tightly
shut, now open them. Wasting and weakness of distal muscles with
areflexia. Percussion myotonia: Percuss thenar eminence and watch for
voluntary thumb flexion.
Extra points: Cardiomyopathy (brady- and tachyarrhythmias), diabetes
mellitus due to impaired insulin secretion (ask to dip urine), nodular
thyroid enlargement, peripheral neuropathy may occur in longstanding myotonic dystrophy due to diabetes. In advanced disease,
the degree of myotonia may paradoxically be less obvious.
Inheritance: A trinucleotide repeat disorder, with its mode of
inheritance autosomal dominant with the locus at 19q13.2 - q13.3,
onset in 20s, genetic anticipation (worsening severity of the condition
and earlier age of presentation with progressive generations due to
expansion of tri-nucleotide repeat sequences). Also occurs in
Huntingtons chorea and Fredreichs ataxia. Condition may show
anticipation progressively worsening signs and symptoms.
Differential diagnosis: Facioscapulohumeral dystrophy, limb-girdle
dystrophy and hypothyroidism.
Investigations: CK (2-10x normal), IgG, thyroid function tests, FSH
due to gonadal resistance, ECG: Low voltage P waves, bradycardia,
first-degree block or more complex disorders. EMG: Demonstrate
myotonic discharges evoked by movement of the electrode; myopathic
potentials are recorded from weakened and wasted muscles during
volitional movement. Muscle biopsyfrequent long chains of nuclei
are seen in the middle of muscle fibres; these changes are seen more
marked postmortem.
Management: Weakness is a major problem no treatment,
procainamide/phenytoin may help myotonia, advise against general
anaesthetic, fit a pacemaker for symptomatic bradycardia.
SYRINGOMYELIA
This 40-year-old man has weak hands. Examine his upper limbs and
suggest why.

Syringomyelia is caused by a progressively expanding fluid-filled
syrinx within the cervical cord, typically spanning several levels.
Frequently associated with Arnold-Chiari malformation and spina
bifida.
Weakness and wasting of small muscles of the hand.
Loss of reflexes in the upper limbs.
Dissociated sensory loss in upper limbs and chest: Loss of pain
and temperature sensation (spinothalamic) and with preservation
of joint position and vibration sense (dorsal columns).
Scars from painless burns.
Charcot joints: Elbow and shoulder.
Pyramidal weakness in lower limbs with upgoing plantars.
Kyphoscoliosis is common.
Horners syndrome. (ask if you can examine the cranial nerves for
signs of syringobulbia: Loss of pain and temperature sensation on
the face).
Look for evidence of Charcots joints at the shoulder and trophic
changes in the hands.
If the syrinx extends into brainstem (syringobulbia) there may be
cerebellar signs and lower cranial nerve signs.
Investigation of choice: Spinal MRI.
BROWN-SQUARD SYNDROME
suggest why.
There is spastic weakness (monoplegia one limb; hemiplegia
one arm and leg) and enhanced reflexes and loss of propioception
and vibration sense on one side (ipsilateral to the lesion) and loss of
pain and temperature sense on the other (contralateral to the lesion).
True Brown-Sequard syndromes, with 50% hemisection, are rare.
Causes are same as those described for a spastic paraparesis.
Demyelination and degenerative vertebral disease are the commonest
causes. Ask about evidence of decompensation including bladder
or bowel symptoms.
MUSCULAR DYSTROPHIES
suggest why.
189
Table 6.2: Types of muscular dystrophies.

Type
Features
Severe X-linked
Duchenne
muscular
dystrophy
Presents 3rd year of life, May be low Death towards end of second
severe proximal
decade
weakness of lower
limbs, calf hypertrophy,
cardiac muscles affected,
onset 5th-25th year
Benign X-linked
Becker type
muscular
dystrophy
Weakness and wasting of Normal

pelvic and shouldergirdle muscles
Many survive to normal age
Facioscapulohumeral
dystrophy
Often in adolescence.
Normal
Facial weakness:
prominent ptosis.
Difficulty in closing eyes.
Normal life span. The mode

of inheritance is autosomal
dominant, both sexes equally
affected. The gene is
Speech is impaired owing

to difficulty in articulation
of consonants.Wasting
of sternomatoids,
lower pectorals, triceps,
biceps. Marked scapular
winging. Occasionally
deltoids hypertrophy to
compensate.
to the long arm of

chromosome 4.
Onset usually in second Normal

or third decade.
Weakness and wasting
may begin in either
shoulder or pelvic
girdle muscles. Hip
flexors and glutei are
weak. There is early
wasting of medial
quadriceps and tibialis
anterior. Hypertrophy
of calves and/or deltoids
may occur. Ankle jerks
preserved. The face is
Often severely disabled by

middle life with death before
normal age. Autosomal
recessive.
associated
Limb girdle
muscular
dystrophy
IQ
Prognosis
never affected.
To demonstrate facial-scapulo-humeral dystrophy, if having been

asked to examine the upper limbs, you should specifically demonstrate
facial weakness (for example by asking the patient to scrunch up their
eyes or to blow out their cheeks). It is also important to expose the
trunk properly (this may involve asking the patient to take his shirt
off).
CERVICAL MYELOPATHY
Patients present with chronic weakness of the lower limbs and loss of
sensation; bladder or bowel disturbance can occur; sensory symptoms
in the lower limb are not always present, even with clear signs; painful
cervical spine even with clear signs. Clasp-knife spastic legs with
preserved bulk, clonus at the ankle + knee, weakness in a pyramidal
distribution, hyperreflexia (in the lower limbs, Babinksis sign), dorsal
column (vibration and cutaneous sensation before proprioception) or
spinothalamic loss, loss of abdominal reflexes. In the upper limbs often
asymmetrical reflexes, inverted reflexes of the mid-cervical reflex pattern.
The signs in the upper limbs are often not marked; wasting of the small
muscles does not occur unless there is a radiculopathy affecting C8 or
T1.
Aetiology: Cervical spondylosis degenerative disease is usually
most pronounced in the mid-cervical region at C5/6.
Differential diagnosis: Demyelination, syringomyelia (dissociated sensory
loss + bulbar signs). Investigations: Cord needs imaging, measure
B12.
Management: Consult with a neurosurgeon for myelopathy at one level
or multiple levels due to diffuse narrowing of the canal. Conservative
management with a collar, only if surgery is unsuitable. Inverted
reflexes are the extension of triceps when the biceps is tapped and
finger flexion when supinator is tapped. Biceps and supinator jerks
may be absent due to damage at C5/6, whereas the triceps and finger
jerks are brisk because their reflex arcs lie below the level of the lesion.
This is the mid-cervical reflex pattern.
Extensor Plantars and Absent Knee Jerks

This 40-year-old man has weak hands. Examine his lower limbs and
suggest why.
- Fredreichs ataxia
- Subacute combined degeneration of the cord
- Motor neuron disease
- Taboparesis
- Conus medullaris lesions.
Combined upper and lower pathology, e.g. cervical spondylosis
with peripheral neuropathy.
191
MYAESTHENIA GRAVIS
Examine this patients cranial nerves. She has been suffering from
double vision and dry eyes.

Peak incidence: 4th decade, Women 2x as affected as Men.
Clinical signs: Bilateral ptosis (can be unilateral), the head may be held
back, the patient looking down their nose to counteract the ptosis,
complicated bilateral extra-ocular muscle palsies, expressionless face/
myaesthenic snarl (on attempting to smile), diplopia on holding the
extremes of gaze, inability to read aloud or count continually (the
voice becoming quiet), nasal speech, palatal weakness and poor
swallow (bulbar involvement in around 10% of patients), demonstrate
proximal muscle weakness in the upper limbs, particularly neck
weakness on holding the head up from the pillow,and fatiguability
(10% of patients) (reflexes are normal), shoulder weakness > pelvic
weakness, sensation normal, bulbar weakness can lead to regurgitation
of fluids, respiratory weakness, look for sternotomy scars.
Associations: Other autoimmune diseases, e.g. diabetes mellitus,
rheumatoid arthritis, thyrotoxicosis and SLE, and thymomas. Causes:
IgG anti-nicotinic acetylcholine receptor antibodies affect motor endplate neurotransmission. Titre of antibody does not correlate with
disease activity or progression. Many patients have thymic hyperplasia
especially those with AChR antibodies. Thymic hyperplasia is present
in 70% of patients under 40-years of age. These patients have an
increased association with HLA B8 and DR3.
Exacerbating factors: Pregnancy, hypokalaemia, over-treatment, change
of climate, emotion, exercise, certain drugs (e.g. aminoglycosides,
penicillamine, -blockers).
Tests: (a) Edrophonium (Tensilon) test: An acetylcholineesterase
inhibitor increases the concentration of ACh at the motor end plate
and hence improves the muscle weakness. Can cause heart block and
even asystole. Two syringes are prepared, 10 ml Normal saline and
10 mg edrophonium with 10 ml. Give 2 ml of each IV injection.
Observe. It is positive only if edrophonium improves muscle power
(b) AChR antibodies (and also striated muscle antibody) (90%
specificity, 100% sensitivity). (c) Vital capacity. (d) EMG: Characteristic
decrement in the evoked muscle action potential following stimulation

of the motor nerve (e) CXR mediastinal mass, (f) CT or MRI of the
mediastium to look for a thymic mass.
Cholinergic crises: Salivation, lacrimation, urination, diarrhoea, gastric,
emesis, small pupils. The features which distinguish myaesthenic crisis
are response to edrophonium and absence of cholinergic phenomena.
Treatments: Acute (I/V immunoglobulin or plasmapharesis), chronic
(acetylcholine esterase inhibitor, e.g. pyridostigmine,
immunosuppression: steroids and azathioprine (the steroid-sparing
agent of choice), thymectomy is beneficial even if the patient does not
have a thymoma), ice on closed lid for 2 minutes will improve ptosis
by at least 2 millimetres. Bone densitometry is advisable for patients
commencing long-term corticosteroids. Plasma exchange can be tried
in emergencies (e.g. respiratory difficulty/facility to intubate and
ventilate should be available).
Lambert-Eaton myaesthenic syndrome: Diminished reflexes that become
brisker after exercise, lower limb girdle weakness, associated with
malignancy, e.g. small-cell lung cancer, antibodies block pre-synaptic
calcium channels, EMG shows a second wind phenomenon on
repetitive stimulation.
WASTING OF THE SMALL MUSCLES OF THE HAND

This 56-year-old lady has noticed wasting in her hands. Please examine
her upper limbs and discuss.
Remember that rheumatoid arthritis and old age are common causes
of this. First establish whether the wasting and weakness is generalised
or whether it is restricted to the muscles supplied by the median or
ulnar nerves (test abductor pollicis brevis and interossei). NB.
Combined median and ulnar nerve lesions will of course produce
generalised weakness and wasting but this is rare; distal muscular
atrophy is another rare peripheral cause. Test for any sensory deficit
and fasciculations, and look carefully for signs of rheumatoid disease.
If the disturbance is generalised the lesion is likely to be central,
i.e.
Lesions of the cord affecting T1, e.g. Motor neurone disease,
syringomyelia, spinal cord tumours.
Lesions affecting T1 root, e.g. Neurofibroma, cervical spondylosis
(relatively rare at this level), apical lung tumours.
193
Lesions of the brachial plexus affecting T1, e.g. Klumpkes paralysis,

cervical ribs, Pancoast tumour.
Peripheral nerve lesions, e.g. median and ulnar nerve lesions
You should therefore:
Look for fasciculation in the hand and arm (prominent in motor
neurone disease: if you suspect the diagnosis proceed).
Test for loss of reflexes and spinothalamic sensation in the arm.
Test sensation over T1 dermatome.
Palpate for cervical ribs.
Observe for Horners syndrome.
Look for a site of ulnar nerve damage at the elbow.
Cranial Nerve Disorders: A quick reminder.
The candidate should be able to examine each of the cranial nerves
(in sequence), and to recognize and discuss the pattern of abnormal
signs.
General inspection
Ramsay-Hunt syndrome. Herpes zoster visible in the outer ear,
together with a facial palsy and/or hearing loss.
Benign intracranial hypertension: Short, obese, hairy women with
papilloedema.
Acromegaly associated visual field defects.
Graves disease impaired extra-ocular movements, secondary to
nerve palsy.
1. Has there be a change in the sense of smell or taste? suspect
anterior cranial fossa floor fracture, frontal tumour or Kallman
syndrome (genetic cause of anosmia and infertility). This is not
likely to be appropriate for examination.
2. Visual acuity using a Snellen chart (other means include counting
fingers, perception of movement, perception of light), and then
exclude red-green colour blindness (Ishihara), as patients with
demyelination may have obvious impairment in both. If visual
acuity is impaired: Is this correctable with spectacles or a pinhole?
If you think the patient is near-blind, then establish if movement
and light can be detected.
Pupil Reactions
Test for afferent papillary defect, preferably using the swinging light
test (greater constriction with a consensual response than a direct
light response). This defect may be caused by lesions of the retina

(including severe macular degeneration), optic nerve, chiasm and optic
tract. It is particularly associated with optic nerve damage in multiple
sclerosis. The papillary response is also known as a Marcus-Gunn
pupil. When the normal eye is stimulated by a bright light, the pupil
constricts and remains constricted. In contrast, the pupil of the affected
eye reacts slowly, less completely and transiently, so that it may start
to dilate again even while the light is shining on it the so-called
papillary escape phenomenon. The reaction is best seen if the light is
rapidly alternated from one eye to the other, each stimulus lasting 23 seconds, with a second between. While the normal pupil constricts
and stays small, the abnormal pupil dilates instead of constricting as
the light falls on it.
Check the size and shape, symmetry, reaction to light direct and
consensual reaction, accommodation.
The candidate should be able to discuss Horners syndrome, a
tonic pupil and Argyll-Robertson pupil.
HORNERS SYNDROME
Reactions to light and accommodation should be present and normal.
Look at the ipsilateral side of the neck for scars (trauma e.g.
central lines, carotid endarterectomy surgery or aneurysms) and
tumours (Pancoasts tumour).
Examine for weakness of the small muscles of the hand (T1) and
for loss of sensation over the T1 dermatome.
Test for loss of pain and temperature in the arm and face, loss of
arm reflexes, bulbar palsy and nystagmus (syringomyelia/
syringobulbia).
Tell the examiner that you would like to examine the chest
clinically and radiologically for evidence of a Pancoasts tumour.
Cause: Following the sympathetic tracts anatomical course
(brainstem: MS, stroke), spinal cord (syrinx), and neck (aneurysm,
trauma, Pancoasts tumour). Congenital Horners syndrome: Iris
is of different colours (heterochromia).
TONIC (HOLMES-ADIE PUPIL)

A unilateral dilated pupil is striking.
Look for ptosis and test ocular movements for evidence of a
IIIrd nerve palsy (the main alternative diagnosis).
Test the response to light (very slow) and accommodation (also
slow but more definite).
195
Figure 6.4
Also ask the examiners permission to test the ankle jerks (absent
or diminished ankle and knee jerks are expected).
Mention that another cause are mydriatic eye drops.
A Holmes: A die pupil constricts promptly to 2.5% metacoline.
Discussion: A benign condition that is more common in females.
Reassure the patient that nothing is wrong.
ARGYLL-ROBERTSON PUPILS
Figure 6.5
Pupils are small and irregular and react to accommodation but

not to light.
Look for wrinkled forehead with ptosis and absent ankle jerks,
loss of joint position sense and vibration sense, positive Rombergs
test and sensory ataxia, Charcots knee joint and aortic
incompetence.
Cause is a lesion in the tectum of the midbrain.
Usually a manifestation of quaternary syphilis, but it may also
be caused by diabetes mellitus, orbital injury, hereditary
neuropathies and sarcoidosis.

Test for quaternary syphilis using TPHA or FTA, which remain
positive for the duration of the illness. Treat with penicillin.
Aniscoria (NO CAUSE) Bilateral constricted pupil (elderlynormal
finding).
Visual Field Testing

Central and peripheral fields with a 10 mm red pin. Assess the
visual fields by comparing the patients with your own. Ask the
patient to look at your nose, and while you cover one eye determine
if the visual field of the other is within the limits of your own. It is
best for you to close your ipsilateral eye and for you to cover the
patients ipsilateral eye, to ensure that the eye is completely
covered.
Central scotoma: This is usually found using a red pin. Hint: If a
patient complains of a hole in his visual field, it is often easier to
give him the pin and ask him to place it in the hole in his vision.
Causes of a central scotoma: Retrobulbar neuritis most commonly
in cases of multiple sclerosis, choroidoretinitis, pressure on the
optic nerve by a tumour, optic atrophy due to toxins or vitamin
B12 deficiency.
Bilateral hemianopia and homonymous hemianopia can be found
using confrontational visual field testing. When using a red pin,
ask the patient to tell you when the pin is seen as red. Ensure the
pin is midway between your eye and the patients eye and compare
the patients field to red with your own. A lesion at the optic
chiasm (e.g. pituitary or suprasellar tumour) results in bitemporal
hemianopia, while a lesion of the optic tract produces homonymous
hemianopia.
Figure 6.6
197
It may be relevant to map out the blind spot. Cover your left eye
and tell the patient Could you please cover your right eye with your
right hand (pause to let them do this.) Thank you, could you fix your
gaze on the bridge of my nose again. I am going to slowly move a red pin in
front of you. You will see the pin disappear and then reappear again. Please
tell me when you first notice it go and then when you see it again. Now
bring the pin slowly across your visual field midway between you
and the patient. Compare the size of your blind spot with the
patients. A central scotoma occurs with defects in the retina or
optic nerve.
Optic fundi: Perform fundoscopy by first looking at the anterior
chamber then the lens and finally the retina itself. Is there disc
cupping (glaucoma) or blurring of the otherwise clear margins
(papilloedema)? Are the discs pale (optic atrophy)? [See Station 5].
Are there any retinal changes of diabetes or hypertension?
III, IV, VI 3 = oculomotor, 4 = trochlear, 6 = abducens.
Ptosis seen with both Horners syndrome and III nerve palsy.
Palsies and Ptosis

Causes of bilateral ptosis: Myotonic dystrophy, myaesthenia gravis,
ocular myopathy, bilateral Horners syndrome due to
syringomyelia, syphilis (Argyll-Robertson pupils). Causes of a
unilateral ptosis. Complete IIIrd nerve palsy (complete ptosis, pupil
large, divergent strabismus, diplopia on adduction), partial IIIrd
nerve palsy (partial ptosis with a large pupil on the affected side),
Horners syndrome.
Investigations of ptosis: Glucose (diabetes mellitus), ESR/CRP
(mononeuritis multiplex), anti-AChR antibodies, CXR (apical
malignancy/cervical rib), syphilis serology, MRI, EMG.
Exopthalmos: When gross will result in impaired ocular movements.
Best assessed together by asking the patient to focus on your finger
(kept about a metre away) as it moves horizontal and vertical
extremes noting the full range of movement in each eye, and asking
the patient if there is any double vision. If the patient does see
double establish which eyes movement is responsible by covering
each eye in turn at the point of double vision. The eye from which
the most distant image disappears when covered is the one with
the impaired muscle.
Check the function of individual oculomotor nerves. Candidates
should be able to make a general assessment of external ocular
movements by getting the patient to fixate on an object and follow

it in a H pattern. On inspection, III and VI nerve palsies may be
obvious. You must quickly demonstrate which nerves are weak
and the direction in which reported diplopia is maximal. In less
obvious cases, you should be able to analyse the diplopia by using
the cover test (when looking in the direction of action of the weak
muscle, the outer image disappears on covering the affected eye).
In the case of a III nerve palsy, you must state whether the lesion
is complete or partial. In a complete lesion there is complete ptosis,
the eye is deviated downwards and outwards with loss of upward,
downward and medial movements, and a dilated unreactive pupil.
It is obviously necessary to elevate the eyelid to observe the latter
findings because of the ptosis. Note that in vascular lesions of the
III nerve (e.g. in diabetes, arteriosclerosis or arteritis) the pupil
may be spared.
You should demonstrate whether the IV nerve is intact by lifting
the eyelid and asking the patient to look down: If the nerve is
intact there will be intorsion of the eye. Test lateral gaze to confirm
that the VI nerve is intact.
You may be asked the likely cause: Remember that the commonest
causes of a pure III nerve palsy are posterior communicating artery
aneurysm, diabetes, atherosclerosis and raised intracranial
pressure. The latter three are also common causes of a VI nerve
palsy.
Remember that the III, IV and VI nerve palsies may be affected
singly or in combination as part of a cranial neuropathy due:
Diabetes, polyarteritis nodosa, multiple sclerosis, sarcoidosis, basal
meningitis: Tuberculous, syphilitic and carcinomatosus.
Look specifically for internuclear ophthalmoplegia (failure of
adduction in one eye and nystagmus in the abducting eye) and
causes (multiple sclerosis, vascular disease, tumour such as pontine
glioma, inflammatory lesions of the brainstem, drugs such as
phenytoin and carbamazepine). Investigations include MRI scan.
The lesion is in the medial longitudinal bundle which connects the
sixth nerve nucleus on one side to the third nerve nucleus on the
opposite side of the brainstem. The eye will not adduct because
the third nerve, and, therefore, the medial rectus have been
disconnected from the lateral gaze centre and sixth nucleus of the
opposite side.
Nystagmus:
Nystagmus is defined as a slow drift in one direction with a fast
correction in the opposite direction.
199
Key signs: Lasting <2 beats on extreme gaze normal; involuntary

usually jerky eye movements; horizontal often due to vestibular
lesion acute away from lesion/chronic towards lesion; cerebellar
lesions nystagmus towards the affected size; if greater in eye that
is abducted, there may be an intranuclear ophthalmoplegia suspect
MS.
The direction of nystagmus is defined by the direction of the fast
phase. The slow phase is the pathological component; the fast phase
is the correction. Some neurologists also grade nystagmus into:
Grade 1 (present in looking in one direction only), grade 2 (present
with the eyes in the neutral position), and grade 3 (present on
looking on either side). Ataxic nystagmus is a popular case so be
sure that you can demonstrate the signs (nystagmus in the
abducting eye often associated with weakness of adduction due
to internuclear ophthalmoplegia). For horizontal nystamus which
occurs only on looking laterally, the direction of the fast phase is
away from the lesion in a peripheral lesion, but towards the lesion
in a central lesion.
Tinnitus may imply Menieres, varies with head position implying
benign positional vertigo. Up and down nystagmus midbrain or
4th ventricle lesion. Investigations: Appropriate to the possible cause.
Management: As for cause.
Pendular nystagmus is symmetrical moving at the same speed in
both directions. Jerk nystagmus has a fast phase in one direction
with a slow phase in the other. The type of nystagmus is ascertained
by this flow diagram:
Aetiology: Peripheral lesions (labyrinth/vestibular apparatus),
central lesions (brainstem or cerebellar pathology).
Prolonged horizontal nystagmus on lateral gaze commonly drugs
(e.g. phenytoin, barbiturates, benzodiazepines and alcohol) and
demyelinating disease.
Vertical nystagmus: Upbeat Wernickes encephalopathy, MS,
brainstem tumours; downbeat tumours at the foramen magnum
(where a cerebellar lesion is suspected, look for other cerebellar
signs).
Ataxic nystagmus is closely allied to INO.
Pendular nystagmus: No fast phase and due to congenital or retinal
pathology (e.g. albinism); therefore, examine visual acuity and
examine the fundus.

Investigations: Audiogram, caloric tests (peripheral VIIIth nerve
function), MRI (lesions), phenytoin level, alcohol, LFTs, red cell
transketolase (Wernickes encephalopathy).
Management: Dependent on the cause.
V Shingles: Reactivation of latent trigeminal nucleus zoster may be
associated with dysaesthesia.
The ophthalmic and maxillary divisions carry only sensory fibres,
the mandibular division carries additional motor fibres. Test for
jaw opening, teeth clenching and horizontal jaw translocation, along
with sensation in the face (know the quintothalamic distribution).
Cutaneous distribution of the three components: You should test
light touch and/or pinprick in the three divisions of the V nerve
(ophthalmic, mandibular and maxillary); compare one side with
the other, right or left.
Jaw Jerk
Inform the examiner you would like to perform the corneal
response.
Masseter (Clench your teeth), temporalis, ptyergoid muscles
(Open your mouth and dont let me close it).
In a cerebellopontine angle syndrome, any combination of cranial
neuropathies involving the trigeminal, facial and vestibulocochlear
nerve may occur. Corneal reflex loss is often the first sign, followed
by facial sensory loss. Facial weakness can be late sign. There may
be nystagmus. There may be sensorineural deafness.
Cerebellopontine angle lesions, including acoustic neuromas and
meningiomas, may cause slowly progressive hearing loss or
tinnitus. Vertigo is a rare or late sign. The next step is
neuroimaging. The cerebellopontine angle is the angle between
the cerebellum, lateral pons, and petrous bone. Cranial nerves 5-8
emerge from it from the pons in cranio-caudal sequence.
VI.The facial muscles are served by the facial nerve. The facial nerve
is almost entirely a motor nerve, supplying all of the muscles of
the scalp and face except the levator palpebrae superioris.
Upper and lower motor neurone facial palsy.
Smile, Show me your teeth, Blow out your cheeks like this,
Screw your eyes up tightly.
LMN facial palsy (e.g. altered taste, hyperacusis, altered
lachrymation as the parasympathetic fibres in the greater superficial
petrosal nerve are interrupted).
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Lower motor neurone palsy has paralysis of the upper and lower
face, so that the eye cannot be closed.
Unilateral facial nerve palsy: Unilateral facial droop, absent nasolabial
fold and forehead creases, unilateral inability to raise the eyebrows
(frontalis), unilateral inability to screw the eyes up (orbicularis
oculi) and smile (orbicularis oris).
Palpate for parotid enlargement (the VII nerve may be involved in
a malignant tumour).
Inspect the external auditory meatus and fauces for vesicles
(Ramsay-Hunt syndrome) and the tympanic membrane for evidence
of otitis media (a rare cause today).
Tell the examiner that you would like to ask the patient whether
he has become unilaterally intolerance to high-pitched or loud
sounds (hyperacusis due to paralysis of the stapedius muscle) and
that you would normally test taste sensation on the anterior twothirds of the tongue (involvement of the chorda tympani).
Look for evidence of corneal damage, conjunctivitis or lateral
tarsorrhaphy.
Level of the lesion:
Pons (MS, stroke) + VIth nerve palsy and long tract signs.
Cerebello-pontine angle + V, VI, VIII, cerebellartumour, e.g.
acoustic neuroma.
Auditory/facial canal + VIII, cholesteatoma and abscess.
Neck and face + scars and parotid mass tumour, trauma.
Commonest cause is Bells palsy: Rapid onset (1-2 days), HSV-1
implicated, induced swelling and compression of the nerve within
the facial canal causes demyelination and temporary conduction
block. Treatment: steroid and acicyclovir. Remember eye
protection. 85% make a full recovery.
Other causes of a VIIth nerve palsy: Herpes zoster (Ramsay Hunt
syndrome; reactivation of herpes zoster in the geniculate gangion),
mononeuropathy due to diabetes, sarcoidosis or Lyme disease,
tumour/trauma, MS/stroke (the long intrapontine course from the
nucleus makes the nerve vulnerable), cerebellopontine angle lesion,
parotid swellings, cholesteatoma (epithelial cells accumulate behind
the tympanic membrane: Needs urgent appraisal by an ENT
surgeon), Millard-Gubler syndrome (Vith and VIIth nerve palsy
and contralateral hemiplegia).
Bilateral facial nerve palsy is very easy to miss but the patient has
an expressionless face. Causes of a bilateral facial palsy: GuillainBarre, Lyme disease, facioscapulohumeral dystrophy, dystrophia

myotonica or myaesthenia gravis, Parkinsons disease (akinesia
rather than weakness), bilateral Bells palsy, sarcoidosis and
myasthenia gravis.
Consider also causes of mononeuritis multiplex.
Investigations: None for Bells palsy, EMG done at 1-2 weeks after
the onset can demonstrate axonal degeneration in up to 15% of
those with a total paralysis, CT brain (UMN lesions where stroke
is likely), MRI (cerebellopontine angle tumour, demyelination,
brainstem stroke), ultrasound (parotid tumours), serum ACE
(sarcoidosis), AChR antibodies (myaesthenia gravis).
Management: Bells palsy (corticosteroids, lateral tarsorrhaphy),
Ramsay-Hunt (acicyclovir, prednisolone to reduce post-herpetic
neuralgia). Stroke and tumours need investigation and treatment
along standard lines.
VII. Hearing
A crude whisper is insufficient at the level of MRCP especially if
the diagnosis is a cerebellopontine angle tumour. Perform Webers
and Rinnes test.
For Webers test, sound is referred to the deaf ear in conductive
deafness, and to the better ear in sensorineural deafness.
For Rinnes test. BC>AC in the deaf ear in conductive deafness,
but AC>BC in both ears in sensorineural deafness.
Further features in a patient with unilateral deafness: Ipsilateral
facial weakness, depressed facial sensation or a depressed corneal
response
Lateral medullary syndrome (Wallenbergs syndrome) or
posterior inferior cerebellar artery syndrome. There is ipsilateral
Horners syndrome (disruption of the sympathetic tract),
cerebellar signs (cerebellum and its connections), palatal paralysis
and diminished gag reflex (IXth and Xth nerves), decreased
trigeminal pain and temperature sensation, and contralateral
decreased pain and temperature sensation (spinothalamic tract).
Involvement of the nucleus and tractus solitarius may cause loss
of taste. Hiccups may occur.
IX. Tonsillar fossa: Gag reflex
The function of the nerve can only be assessed by a painful
stimulus to the tonsillar fossa, and should not be examined.
X. Palatal sounds (e.g. EGG or RUG); the palate moves away from
the side of the lesion.
To assess the patients swallow, they must be fully conscious,
able to follow commands, and be sitting upright. The instructions
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are to take a sip of water, swallow it, the patient says his name,
and observe throughout for coughing or choking.
Palatal deviation: Open your mouth and say aah. The candidate
should be able to recognize palatal deviation, and be aware that
the palate deviates to the intact side in a unilateral palatal palsy.
Jugular foramen syndrome involves the 9th, 10th and 11th nerves
which pass through the jugular foramen (between the lateral part
of the occipital bone and the petrous portion of the temporal
bones). Examination reveals sluggish movement when the patient
says aah on the affected side. Absent gag reflex on the same
side. There is flattening of the shoulder on the same side. Wasting
of sternomastoid. Weakness when the patient moves his/her chin
to the opposite side. Difficulty in shrugging the shoulder on the
same side. Look for wasting and deviation of the tongue (12th
nerve palsy), and tell the examiner you would like to look for
two signs (bovine cough and husky voice).
XI. Spinal accessory nerve (sternocleidomastoid and upper fibres of
trapezius).
For sternomastoids, place one hand on the patients forehead
asking the patient to push the head up off the pillow, and observe
and palpate for the bulk and power of sternomastoids. For
trapezius, ask the patient to shrug shoulders. Observe for
asymmetry.
XII. Tongue (wasting, fasciculation of the non-protruded tongue).
Unilateral palsy (ipsilateral wasting, fasciculation and deviation
to the paralysed side).
A pseudo-bulbar palsy (stiff, immobile tongue).
Communication
Skills and Ethics
(Station 4)
[The MRCP Clinical Examining Board have kindly made available

sample scenarios for this Station: these may be viewed and
downloaded using the following link: http://www.mrcpuk.org/
PACES/Pages/PACESscenarios.aspx]
INTRODUCTION TO THE GENERAL APPROACH

OF THIS STATION
Station 4 aims to assess the candidates ability to guide and organize
a consultation with a subject who may be a patient, relative or
surrogate, such as a health care worker. The candidate is expected to
provide emotional support, discuss further management of the case
and deal with ethical and legal implications as they arise. The inclusion
of this task in the PACES examination is significant, since the medical
interview is considered central to clinical practice. Doctors are thought
to perform around 200,000 interviews in a professional lifetime.
Communication is therefore the clinicians responsibility, with multiple
influences. It is an essential component of the physician role. Effective
communication builds trust between the patient and the doctor,
improves patient satisfaction, recall, understanding, concordance,
decision-making and disease outcome.
The importance of communication was recently emphasised by
the British Medical Association in an article entitled Communication
Skills education for doctors: an update (November 2004) and the
Royal Colleges of Physicians themselves, Improving communication
between doctors and patients (Royal College of Physicians of London,
1997). All patients irrespective of race, gender and social class are
entitled to good standards from their doctors. The essential tenets
underlying this good practice are: professional competence, good
relationships with patients and colleagues, and thinking ethically about
Communication Skills and Ethics (Station 4)
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decisions regarding patients and colleagues. In this chapter, we are

obviously unable to cover all eventuality in the examination. Rather,
we have used 24 scenarios to outline the fundamental principles of
communication skills and ethics which cover the key areas of the values
tested, including breaking bad news, confidentiality and consent,
explaining diagnosis and treatments, different styles of patient
response, and end-of-life decisions (Sections A-G of this chapter).
The RCP want a Registrar that they feel is competent to deal with
such scenario so that the patient/family will be satisfied with the
explanation they are given. It is not possible to try and prepare for all
possible scenarios.
Instead, make sure you have:
A broad knowledge of general medicine.
Knowledge of (national or international) clinical guidelines and
protocols: Useful guidelines relevant to this station are the DVLA
guidelines, NICE guidelines, details about coroner referral, and
BMA guidelines on DNAR.
Intimate knowledge of acute medical management protocols for
common medical emergencies.
A management plan for all common non-acute conditions.
Knowledge of major trials that have altered clinical practice in
some way.
An idea of any topical newspaper reports on medical subjects.
Candidates are not expected to have a detailed knowledge of
medical jurisprudence. For overseas candidates in the UK, detailed
knowledge of UK law is not required, although candidates should be
aware of general legal and ethical principles that may affect the case
in question.
PRINCIPLES OF COMMUNICATION SKILLS

Structure of the Consultation for the Examination
In the examination, five minutes are allowed for reading the referral
letter, 14 minutes for talking to the patient, 1 minute for the candidate
to collect his/her thoughts and five minutes discussion with the
examiner. Read the scenario carefully before going in, decide the
important issues that you are addressing and what you should stress
for the patient to take home. Make sure that you write the main points
you want to discuss otherwise you may forget once you go inside
that room. You are given a blank sheet of paper to scribble on. If
possible, use this time to decide which words are likely to constitute

medical jargon and think of equivalent words a lay person would
understand. When in the room, take a short time to establish rapport,
and lead/direct the interview without being too controlling. See if
the chair has been left a bit further away from the patient; see if there
is a barrier between you and the patient. One of your colleagues tried to
bring the chair around the table near the patient to break bad news and the
examiner said, It is alright. I know what you are trying to do. Point taken.
You are supposed to have, after the 15 minutes, a discussion of 5
minutes when they will ask you questions concerning the case and if
there are any ethical dilemmas. Timing is therefore absolutely crucial
to a decent performance in this Station, and time management, whilst
not explicitly stated, as in real life and indeed for the clinical stations,
can help to determine success. The 5 minutes spent reading the task is
of critical importance.
You should be able to put patients at ease, particularly with regard
to beginning an interview and enabling the patient to raise and discuss
sensitive personal issues. In this station, you should be demonstrate
your ability to adapt their interviewing style to accommodate different
patient styles (overtalkativeness, reticence, depression, hostility,
confusion), the communicative abilities of different patient groups
(e.g. children, patients who understand or speak very little English,
patients with learning difficulties), and the changing demands of the
situation (e.g. within one consultation the candidate may be required
to elicit information about a medical problem, discuss a psychosocial
problem, deal with emotional distress, and provide education). Some
of these issues are discussed in part E of this chapter.
Most of all, you must undertake the task. Do not attempt to convert
the case into something that you would rather do. Each examiner
also has a copy of the written instructions to the candidates, together
with the written subject information and Examiners information. Each
examiner has a structured marking schedule for the case and will
examine independently and without discussion. Be frank with the
patient (honesty means integrity)! You are expected to have agreed a
summary and plan of action with the patient/subject before closure
and discussion.
The structure suggested below is based on the Cambridge-Calgary
formulation. This structure can be applied to virtually all scenarios.
These scenarios may be set in any branch of adult medicine that an
FY2/ST1 is likely to encounter in an in-patient or outpatient setting.
The semi-structured marking schemes involves sections covering
initiation of the interview, appropriate exploration and planning, and
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exploration and problem negotiation, and conclusion of the interview,

as well as the discussion of relevant issues of medical ethics and/or
law. This marking scheme is given below (reproduced by kind
permission of the Federation of the Royal College of Physicians).
This Station can go Easily Wrong!

The new PACES format allows candidates to receive more structured
feedback on why they failed this particular station. This station is an
evolution of the old viva system. The easiest way to ensure that you
are given a clear fail in this section of the exam is by saying something
that is downright dangerous medical practice, or indicates a complete
lack of basic understanding about a subject.
Reasons How the Station Could go Wrong

1. Taking the station for granted: It is very important to see as many
clinical cases as possible in the run-up to the exam both to refine
ones examination skills and to pick up key signs. Nevertheless, to
ignore the communication skills and ethics station nor to devote a
proportion of your time in proportion to the examination is unwise.
2. Not showing enough empathy: It is relatively easy to distinguish those
candidates who are trying to show empathy from those who do
not. It is important that the candidate is seen to demonstrate
empathy in dealing with their situation. Empathy is the ability to
identify or understand with another persons predicament.
Synonymous words include compassion and sympathy. One useful
tip in helping you develop more empathy is to try and imaging
how you would feel if you or a relative were caught up in that
persons situation.
3. Using medical jargon: Do not use medical jargon. Remember that
this station is testing your ability to communicate effectively. You
are not communicating effectively if the person in front of you
who has no medical knowledge cannot understand what you are
saying. Bear in mind that medical jargon is not necessarily limited
to medical terminology but also medical speak. By medical speak,
we mean words that are not for the most part purely medical but
convey a different meaning to health professionals.
4. Misreading the scenario given to them: Read the scenario carefully. In
addition, the information contained in the scenario may be
extremely important, for example, why have they made the patient
a young woman (issues of contraception, pregnancy) or why have

they mentioned that the pastient is attending with their relative
(issue of confidentiality).
5. Being insensitive with patients/relatives: This does not need any
explanation.
6. Volunteering wrong information: Although, this station is not testing
your clinical skills, it is important that the candidate does not
communicate erroneous clinical information. This in itself may lead
to the interview going in a completely different direction to that
intended by the examiners. Examples, include making up
information, not given to the candidate either from the scenario
or from the actor/actress. Another error is assuming that the
patient has had tests not mentioned in the scenario. For example,
although in some scenarios when it says the cancer has metastasized,
it is very likely that you have performed a CT to find out where it
has metastasized. However, some of your colleagues suggested
the patients confusion is secondary to metastases (when the primary
was lung cancer). As you well know, hypoxia or secondary infection
could have caused the confusion.
SECTION 1: CONDUCT OF THE INTERVIEW

The first third of the structured marking scheme is devoted to the
general conduct of the interview, in particular, an appropriate initiation
followed by adequate exploration of the patients beliefs, concerns
and expectations.
Initiation
Introduction of doctor to patient; introduction as Dr.
Establish reason for the discussion/explain role clearly.
Agree the purpose of the interview with the patient: Ask the patient
what he/she wants or needs.
Put the patient at ease and establish good rapport. Ways in which
to develop good rapport include accepting non-judgementally what
the patient says, acknowledging the legitimacy of the patient to
hold their views (I can understand that you wish to get checked
out). It is vital not to be too judgemental, patronising or
paternalistic.
Make appropriate eye-contact early in the interview. General
principles of non-verbal communication include appropriate bodyposture, proximity, touch, body movements, facial expression, eye
behaviour, vocal cues, use of time, physical presence, and
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environmental cues. Use non-verbal cues to demonstrate

attentiveness and build the relationship. Patients and examiners
alike are good at picking up non-verbal cues.
Explanation and Planning

Explanations should be tailored to the patients preferences in terms
of the amount and timing of the information provided.
Assess the patients level of knowledge,
Assess the patients concerns,
Assess the patients expectations and feelings.
You need to assess the patients starting point. Discover what the
patient already knows, is fearful of, and what they are hoping for,
particularly when they are frightened. The rewards of obtaining an
accurate picture of where the patient and their relative is coming from
before giving information about prognosis or treatment options are
great. Gauging how much the patient wishes to know also requires
skill. Do not fall into the trap of doing most of the talking (this is a
mistake that leads to failure). Remember that the actor in front of you
will have been given information that would not be initially available
to you and can only be gleaned by asking relevant questions. In
addition to that, it is a well known fact that listening is respectful and
polite. Try not to interrupt.
Beliefs
Were here to talk about X. Is that correct?
What do you think is causing it?
Why do you think that might be happening?
Have you had any ideas about this yourself?
Have you got any clues or theories?
Youve obviously given this some thought; it would help me to
know what you think it might be?
Is there anybody else you know who has this problem?
Concerns
What are you concerned that it might be?
Is there anything particular or specific that you were uneasy
about...?
What was your worse fear or thoughts about this?
In your darkest moments what had been going through your
mind?
Is there anything else that you would like to talk about?
Expectations
How were you hoping I might help you with this?
What were you hoping we might be able to do for this?
What do you think might be the best plan of action?
Youve obviously given this some thought, what were you thinking
might be the best way of tackling this?
What sort of information do you want to know?
Feelings
How has all of this made you feel?
How has this left you feeling?
How have things seemed to you?
In the subsequent part of the interview, you will be expected to:
Demonstrate empathy, response and non-judgemental attitude.
Empathy is the understanding and sensitive appreciation of another
persons predicament or feelings, and the communication back to
the patient.
Give the information required in simple language avoiding medical
jargon, abbreviations or slang.
Inform the patient about the options as to what can be done or
should be done and what you are going to.
Avoid patronizing the patient by talking extremely slowly or
loudly, calling them dear or saying sure, sure dismissively.
Check out non-verbal cues this allows doctors to express empathy
and compassion for the patients position. It also gives the doctor
space to enquire about further concerns and respond to them with
feeling. I can see that you look very distressed to hear the results of the
tests confirm your worst fears. I am extremely sorry (pause) you mentioned
your husband is diasbled; have you any other concerns you wish to discuss
now? or The last point made you look worried. Is there something more
serious about the point you would like to tell me?
Encourage active listening: Wait time, facilitate responding
(encouragement, repetition, paraphrasing), and encourage nonverbal transmission.
Facilitate questions and answer them, but avoid distressing too
much.
Prioritise problems.
Redirect interview as necessary with sensitivity.
Offer support in terms of concern, understanding, willingness to
help, partnership and sensitivity.
Some golden rules of things of what not to do!
211
Do not talk over the patient; if it is necessary to interrupt, do it

sensitively and rarely.
Do not get angry with the patient if they cannot remember things
or do not accept your views.
Do not use statement questions, such as You dont have diabetes?
SECTION 2: EXPLORATION AND PROBLEM NEGOTIATION

The next section of the marking scheme assesses the ability of the
candidate to agree a clear course of action, involving achieving an
appropriate diagnosis and treatment plan, and to summarise and check
the patients understanding. It is expected that the candidate within
14 minutes concludes the interview appropriately, without
overrunning. A possible way in which these goals can be achieved is
suggested below:
Use an appropriate questioning style (generally open-ended to
closed as the interview progresses).
First it is a good idea to start with encouraging the patient to
contribute their thoughts first and its useful to be forewarned
about potentially strong feelings against a course of action, before
rather than after, it has been suggested.
Doctor: Before I suggest a way Id like to hear what you had in
mind or anything you wouldnt be keen to consider?
Patient: Ive heard a lot about the dangers of surgery and Im not
too keen on being reliant on drugs for the rest of my life. Is there
a homeopathic remedy you can recommend?
Next you should share your own thoughts about management this allows patients to understand your own reasoning as well as
your difficulties and dilemmas. Enlistment is a term that conveys
the initiation of the physician to do this.
Doctor: I can well understand your concerns about medication
but having a blood pressure of this level makes me think it is
unlikely that you will be able to control it by diet and exercise
alone. There might be a risk involved if you exercise vigorously in
the meantime I think the best ways is to. What do you think?
Are these treatments acceptable to you?
Next, you need to provide clear and relevant information about
the various approaches and options continue by involving the
patient by offering choices and making suggestions (not directives).
Doctor: There are clearly pros and cons to each of these options
what preferences do you have?
Patient: Yes I agree Im really not sure now

Doctor: My suggestion is that we get an expert opinion about
your gallstonesand see what this involves what do you think?
Finally - actively seek and encourage their reactions, views and
acceptability about what is proposed and negotiate a mutually
acceptable plan
Doctor: Perhaps we can start with something mild and check to
see if there are any problems before going on Is this acceptable
or do you have any other ideas
Summarise the subjects understanding.
Is there anything else that you are unclear about or didnt
understand?
From what we have talked about today, what do you think is
most important?
I want to make sure, Ive got everything. You are concerned
about.
Formulate a plan of action with the patient.
Reiterate your discussion with the patient to ensure understanding.
Offer co-partnership and support. Overt statements such as we
need to work on this together or I will undertake to speak to the specialist
on your behalf, you will not be left to cope with this on your own how
can we go forward now? are examples of phrasing which may help
patients and need to be underlined.
Ask if there are any important issues not covered or if they have
any further concerns that they would like you to address.
Remember it is often appropriate to say that you would seek senior
or specialist advice.
Offer further information sources, e.g. leaflets, societies, and
support groups.
Close the interview appropriately. Offer a clear follow-up plan,
set a date for a next appointment. Offering to contact relatives or
carers when the patient has expressed concern about informing
others about their diagnosis or prognosis is often helping. This all
arises from the need to inform the patient that the interview is
over.
Common questions that can be expected from the Examiners:
How do you feel that went? Did you put the patient at ease?
What could you have done differently?
Which areas if you had time would you have covered?
What and how do you the patient has taken from your consultation?
They will then discuss legal and ethical issues (see below).
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SECTION 3: MEDICAL ETHICS

In dealing with your case scenario in the examination, you must be
able to communicate your argument with relation to the four
fundamental ethical principles. The examiner will expect you to have
some understanding of these principles which underpin the practice
of good medicine, and may refer to these as part of the semi-structured
oral examination which follows the interview.
Beauchamp and Childress Principles

These four principles derive from Beauchamp and Childress (1979),
and are:
Autonomy: This literally means self-rule, and means in practice
respecting and following the patients decisions in the management
of their condition. Competent patients hace the capacity to think, decide
and act on the basis of such thought and decision, freely and
independently. Respect for patient autonomy requires that health
professionals (and others, including the patients family) help patients
to make their own decisions (e.g. by providing appropriate
information), and respect to follow these decisions (even when the
health professional believes the patients decision is wrong).
Beneficence: This means promoting what is in the patients best interests.
In most situations, respect for the principle of beneficence and for the
principle of respect for patient autonomy will lead to the same
conclusion. The two principles conflict when a competent patient
chooses a course of action that is not in his or her own best interests.
However, a patient can be advised that a course of treatment in her
best interests if there is evidence to do so (e.g. subcutaneous heparin
in a young pregnant lady with a suspected pulmonary embolism, who
is beyond the first trimester).
Non-maleficence: This means avoiding harm. The potential good and
harms and their probabilities must be weighed up to decide what is
in the patients best interests. Sometimes it means that appropriate
safety measures are taken to perform certain essential investigations,
e.g. using an X-ray shield for a CT scan of the chest in a pregnancy
lady.
Justice and sharing: Doing what is good for the population as a whole
in terms of time and treatments. In real terms, this may mean
distributing resources fairly in the provision of care; health

professionals have to decide how much time to spend with different
patients, and decisions must be made about limitations on the
treatments that can be offered at various levels within a health care
system.
In the following sections, general advice is given about the possible
principles being tested, followed by specific examples of tasks which
illustrate these principles.
We have organised these sample scenarios according to the broad
category of their main focus: Breaking bad news, giving information
about diagnoses and treatments, informed consent, differing patient
styles and responses, the ethical issues concerning genetic counselling,
confidentiality and good medical practice, and end-of-life decisions.
We have provided details for the candidate, as well as a description
of a possible consultation in response to that instruction. Of course,
various ethical issues are brought out in these different scenarios. In
the real examination, however, any scenario can be used to examine
your competence at communication skills, law and ethics (e.g. advising
a nursery school teacher not to attend work, even if she wants to,
because of the danger of passing on an infectious disease).
EXAMPLES OF TYPES OF SCENARIOS

Breaking Bad News
A review of candidates experiences of PACES suggests that breaking
bad news has been the focus of many scenarios. Bad news is any
information which is likely to alter drastically the patients view of
the future, for example a diagnosis of multiple sclerosis or the news
that a patient is brain-dead. It is the most potent cause of distress
and, for the medical profession, if done incorrectly, an important cause
of complaints and law suits. Genuine communication is characterised
by attentiveness, listening and dialogue. The required skills can be
learned. Health care professionals sometimes find it difficult to
understand the physical, social, occupational and financial
consequencves of bad news. There are gradations of bad news:
subjective, dependent on individuals life experiences, personality,
spiritual beliefs, philosophical structure, perceived social supports,
and emotional hardiness. A useful structure to this type of task is
given below. We will use a few scenarios which you can use to consider
how these principles may be put into practice.
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A STRUCTURE FOR BREAKING BAD NEWS

Initiation
Use a private setting, involve other health workers, opportunity
for relatives to attend if they wish.
Set your behaviour with correct positioning, eye contact, body
language, listening skills. Some examiners are impressed if you
physically move the chair near the patient, but obviously at a
comfortable interpersonal space.
Check there is privacy.
Ask about attendees.
Offer good eye contact and the patient comfort.
Greet the patient, and obtain the patients name.
Provide a proper introduction of self and role, outline plan for the
consultation.
The clinician should first find out if anything new has happened
since the last encounter. Begin with a neutral question about what
is happening.
Assess beliefs before giving the bad news with appropriate
signposting (signals moving to information).
It is important to hear the patients narrative of events to allow
them to explain what has happened and where they are up to in
their illness, e.g. ask How did it all start? and What happened
next?
Ask about his/her beliefs about the situation. Repeat and reflect
So you had been worried about something like that?Have you thought
about what may be causing your symptoms? or What has been the most
difficult part of the whole thing for you. This way you understand
the patients perspective and what they understand by their illness
and therefore can avoid giving shocking information, if, for
example, it is their belief that they have had curative treatment
when you know that their prognosis is only a few weeks.
Acknowledge what the patient has been told in the past.
You said you wanted me to be honest and open with you. Are you the sort
of person who likes to be told about his medical condition?.
Ask what he/she understood about why a test was done, for
example, Do you know why we did the biopsy?
Give clear signposting/warning shot that serious information is
to follow. Im afraid it looks more serious than we hoped.
Unfortunately, the test results show Give time for the patient to
think about this.

Watch your body language particularly when breaking bad news
look at the patient and lean a bit forwards, pause and
acknowledge distress, recap what has been discussed and check
understanding of the key facts.
Give the bad news simply and clearly in small pieces, without
fudging, in an organised manner.
Build the news up layer by layer.
Reaction and Prognosis

Allow the patient time to respond. There is good evidence that
most doctors interrupt the patient within 30 seconds of speaking.
Encourage the patient to contribute reactions, concerns and feelings.
Be prepared for the patient to have disorderly emotional responses
of some kind and acknowledge them early on.
If the patient is distressed acknowledge this e.g. I can see this news
has really upset you. Can you bear to tell me what distresses you most
about this?. Many patients are distressed but can be uncertain what
the distress is mainly about. Giving permission to discuss concerns
enables the patient to start clarifying the issues and then prioritising
their concerns. This feels like a positive process to the patient and
is always helpful. Avoid premature reassurance or excessive
explanations which can cause dissatisfaction and frustration. Avoid
the use of confusing language and jargon.
Denial is a way of coping with fear and it should be respected as a
coping strategy, especially if the patient is coping. If a patient
declines further information, it should be acknowledged, but also
acknowledge the discomfort of uncertainty and give permission
to ask questions at a later date. Few patients adopt a stance of
denial permanently, most start to ask more information once they
feel more secure. Patients usually experience belief once that they
are able to discuss some of their fears.
Check understanding. Is this making sense? or Have I covered what
you want to talk about?
Repeat certain information.
Keep pausing to allow the patient to think.
Acknowledge the patients concerns and feelings through attentive
listening. Allowing ventilation of feelings provides a therapeutic
part of the dialogue. How does this leave you feeling at the moment?
is the key phrase. The aim is to help the patient try to name their
feelings. Encouraging the ventilation of feelings conveys empathy.
Stay calm and allow time for the person to think about their feelings.
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Discuss prognosis. If the prognosis is unclear, give a range rather

than leave it entirely open, i.e. avoid saying No one can tell for
sure. Be realistic and honest, but try to leave room for hope.
Outline likely consequences in a sympathetic and empathetic
manner.
Treatment
Do not rush into treatment options, if it is clear the patient/relative is
not prepared for the information yet.
Explain clearly the treatment options and outcome, with an
approximate time frame.
Ask for any other or new worries and deal with them
systematically, bring the discussion to a close but offer an
opportunity to speak again and elicit the help of other groups, e.g.
specialist cancer nurses or societies, offer services for the future,
offer transport for the patient. Be prepared for anger and denial,
despair and depression. Consider the long term implications, the
importance of the support network of family, friends and agencies
now and in the future. Identify problems of the patient which are
fixable and make a plan.
Identify coping strategies of the patient and incorporate them.
Identify other sources of support for the patient.
Encourage feedback and check understanding.
Leave room for hope.
Summarise and emphasise what can be done.
Encourage the patient to articulate his personal goals.
Make appropriate arrangements for follow-up contact. Some
examiners like the candidates to enquire what the subject will be
doing in the immediate short-term (e.g. by offering if they are
travelling alone to arrange a cab to go home if the news has been
devestating).
This framework can be applied to the scenarios below, but we
have also included some further details specific to each scenario.
BRAINSTEM DEATH AND ORGAN DONATION

Scenario 1
Problem: Breaking bad news (brainstem death and organ donation).
Subject name: Helen Roberts (sister of the patient, Charles Roberts).
You are the FY2/ST1 for ITU. Charles Roberts is a 28-year-old
accountant who was admitted a week previously following a road-

traffic accident. He was treated for multi-system trauma, and was
being kept alive on a ventilator. The nurses have requested you to
tell the sister of the patient that he has been declared brain-dead by
two consultants. It is documented that he had wished his organs to
be donated to medical science, in a private conversation with his
parents many years ago (obviously without having foreseen these
particular tragic circumstances). Please inform his sister that Charles
Roberts is brain-dead, and approach, if appropriate, the issue of organ
donation.
Introduce yourself and establish a good rapport.
Ask if he would like anyone else there for the discussion. Assess
how much emotional support the subject has in dealing with the
situation.
Acknowledge that it must have been a very difficult time for all of
the family.
Ask what the family has been told in the past, and signpost the
bad news. Explain briefly the history of admission to ITU.
Explain the patient is brain-dead simply. He has technically died
and only the ventilator is keeping the other organs working. For all intents
and purposes, Charles is dead because the parts of the brain vital in keeping
someone alive are damaged beyond any possibility of recovery. Explain
that brain cells cannot be replaced once damaged and so these
cells will not recover. You can also add that if the machines were
to be switched off then his heart and lings would stop. It can also
be helpful to volunteer to involve a neurologist to confirm the
patient is genuinely brain dead.
Explain the next appropriate step is to stop the ventilation. Explain
carefully that this is not to allow her father to die but that
continuing ventilation is inappropriate if a person has already died.
Explain that it is the medical team who makes the decision who
makes the decision as they may think that they are giving you
permission to end his life (you are not actually causing death).
Pause for reflection and allow plenty of time for reaction. Express
condolence.
Show empathy, e.g. I realize that this must be extremely
distressing for you. I only wish that I had better news for you.
Confirm that there is no hope of recovery.
Give opportunity to discuss the situation with family and friends.
According to the subjects response, consider whether a subsequent
discussion regarding organ transplantation would be appropriate.
If so, outline the benefits of organ donation: The shortage of hearts,
219
lungs, kidneys, for example, which may enable other people to

live who would otherwise die. In this case, Charles Roberts, the
patient, had previously suggested the notion that his organs to be
put to medical science.
Nurses in ITU often open the discussion by asking something like
What do you think your mother/sister would have wanted in these
circumstances? I wonder if your father/husband would have wanted his
organs donated for the benefit of others. Remember that this is not an
all-or-nothing situationrelatives, who are legal guardians of the
body, may specify which are acceptable or unacceptable organs
for donation.
If there is strong emotional resistance, then you should respect
and acknowledge their resistance. I can see you find the idea distasteful,
so I wont pursue it any further.
If, instead, the relatives are sympathetic to the idea, you should
explore their reasons and determine whether their reasons are
appropriate are realistic. What exactly makes you support the idea of
organ donation?
Offer him the opportunity to have a discussion with other members
of the family; arrange to meet again in a few hours. Ask the father
if there is anyone else he would like to inform. Ask if he has any
questions. Ensure all staff involved in the case of the fathers
decision.
Arrange a further appointment with somebody.
Mistakes candidates have made when acting out this scenario
including adding information not given to them, e.g. The CT scan
shows a very large bleed or using graphic descriptions of injuries
which are unpleasant.
Definitions
The definitions of death have to some extent varied with altering
technologies. The examiners may be interested in your understanding
of terms such as brainstem death. In 1979, the Medical Royal Colleges
volunteered the definition that brain death represents the stage at
which the patient truly becomes dead. There is no legal definition of
death. Death is now accepted as meaning brainstem death or brain
death. Brainstem death is a deep coma with absent respiration, with
absence of hypoxia, hypothermia, hypoglycaemia, neurolomuscular
blocking agents, acidosis, abnormal biochemistry and sedative drugs.
Tests include fixed dilated pupils, absent corneal response and
vestibulo-ocular reflex. There is no gag reflex or motor response in

the cranial nerves. There is no respiratory effort on stopping the
ventilator and allowing the PaCO2 to rise to 6.7 kPa. The definition
involves two medical practitioners; with two sets of tests; the tests
are repeated at an interval that is left to clinical judgement. A persistent
vegetative state (Jennett and Plum, 1972) is in patients whose
brainstem function persists despite loss of cortical function; there is
no behavioural evidence of awareness of self or the environment.
Their quality of life is at best uncertain, and their life depends on
artificial feeding. There are no reversible causes present, and at least
6 months and usually 12 months have passed since the onset. The
causes are severe head injury (40%), hypoxia (40%), and others. There
are about 600 new cases in the UK. There is brain damage consistent
with the diagnosis. These patients breathe spontaneolusly, open and
close their eyes, swallow and make facial grimaces. However, they
show no behavioural evidence of awareness.
MULTIPLE SCLEROSIS
Scenario 2
Problem: Breaking bad news (multiple sclerosis).
Patient name: Sarah Lewis (aged 26).
Sarah Lewis is a 26-year-old lady who had noticed some numbness of
her feet, with some difficulty in walking, and odd sensations when
taking a bath in her upper limbs, a few weeks ago. You are the FY2/
ST1 in clinic for Neurology. The MRI scan organised by your
Consultant demonstrates multiple peri-ventricular plaques most in
keeping with a diagnosis of multiple sclerosis. Miss Lewis is a local
teacher. She has attended clinic today, and would like the results of
her investigation. On previous occasions, the patient has never asked
what the problem might be and nobody has volunteered a differential
diagnosis. Please discuss with her.
Introduce yourself to the patient and establish good rapport. Ask
if she wishes for anyone else to be present.
Explore the patients understanding of her symptoms and what
they possibly meant, i.e. expectations/suspicions of what may be
wrong.
Ask what she understood by the tests. The patient should be given
small pieces of information in a logical manner; pauses are essential
and give the opportunity for questions. Patients can be given too
much information in one consultation after receiving bad news.
Explain that the MRI scan findings do suggest multiple sclerosis.
Pause to allow this to sink in.
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Watch for her reactions, such as anger or denial. Express empathy.

Ask what she knows about multiple sclerosis (MS). Explain that
myelin is a substance that sheaths around nerves in the body for
insulation. Damage to them is called demyelination and the bare
patches interfere with the smooth conduction of nerve impulses.
Aim to reassure her that there are specialists who look after patients
with multiple sclerosis and that they will help her with the best
available therapy.
How many attacks will I have in a year? Reassure her that she may
have no further attacks.
What happens if I have an attack?. Mention that there is treatment
(iv methylprednisolone) for a sudden attack, but that this usually
requires admission for a few days.
Tell her that there are many people with multiple sclerosis who
lead very active lives. In terms of prognosis, explain that there are
different forms of the disease. Tell her that patients with relapses
and remissions may go on for many years without any major
disability.
Ask if she has any specific concerns; these may include her worries
about future pregnancies, or her ability to hold down a particular
job such as teaching.
Tell her the causes of the condition are unknown.
Explain that there are treatments that prevent the disease from
relapsing, but that these do not affect the final outcome. -interferon
reduce the rate of relapse, but at this point is unlikely to be
warranted.
MS has no effect on fertility and does not affect pregnancy outcome
(but may worsen in the puerperium period).
Offer general advice (polyunsaturated fat may be good, and hot
climate may worsen the condition).
Reassure her that this is not hereditary.
Tell her about the Multiple Sclerosis Society 0800 800 0800. Explain
that joining such groups may allow her to come into contact with
other people who have MS. It may even help her to see other
people who are coping well with the condition. Other advantages
of MS groups in addition to encouragement include educagtion,
tips and awareness of new discoveries.
Ask about her support mechanisms and enquire about his social
circumstances including job. Arrange early follow-up to discuss
this further. Say you will refer her to a specialist and tell her you
will inform her GP.

Conclude the interview appropriately, and arrange a follow-up
appointment. Give her a contact number if she wants to ring you
for advice.
A note on the term multiple sclerosis: this is normally referred to in the
clinical cases as a demyelinating disorder.
LUNG CANCER
Scenario 3
Problem: Breaking bad news (Lung cancer).
Patient name: Michael George (aged 58).
Michael George is a 58-year-old architect. He has smoked 10 cigarettes
a day for the last 40-years. He was admitted a week ago with cough
and shortness of breath. Investigations were normal, apart from a
slightly low serum sodium, and a high resolution spiral CT scan of
the chest demonstrated left-sided hilar lymphadenopathy. The
Radiology report states that the appearance is most suggestive of a
neoplasm of the lung. You are the FY2/ST1 for General Medicine. He
is feeling much better, and would like to go back to work as soon as
possible. You are to discuss with him the results of his investigations,
and their possible significance.
Introduce yourself and establish a good rapport.
Ask the patient what he thought the symptoms meant: Possible
symptoms include cough, shortness of breath, bloody sputum, chest
pain, wheezing or pneumonia.
Ive read a summary from the GP, but what have you been told?
Check what is known already. Is more information wanted? What
is his concern?
Signpost that the news is worse than may first appear (the warning
shot, Faulkner (1998)). Ive had a look at your scans, and its not
good. Ask about why the patient thought he was having tests
and what they mean in the long term, despite the fact he is currently
feeling very much better.
Break the news that he has an abnormal growth of cells in the
lung, a lung cancer. Explain that diagnosis of a lung cancer is
normally through imaging findings (including CXR and CT), as in
his case, but further details about the type of cancer can only be
obtained through further investigation (e.g. induced sputum). The
spread of cancer can be ascertained through further imaging (e.g.
CT of the abdomen). Pulmonary function testing may be useful
for determining suitability for surgery, or safety of further
223
investigation (such as bronchoscopy). It is very important, however,

to absorb jargon.
Ask about the beliefs about the cause. Inform him that 80% of lung
cancers are related to tobacco smoke, and therefore smoking
cessation is advised.
Explain that foreseeing the likely prognosis of his condition
depends upon information from these tests.
Ask the subject if he has any questions. Explain that there will be
appropriate management with the respiratory physicians and
oncologists, and he will be introduced to the physicians and nurses.
Beware of information overload (Greger, 1993) and allow denial,
Im going to be the first person to beat this, Doctor. Youll be proud of
me! Give time for the news to be absorbed, and dont be afraid of
silence. Allow ventilation of feelings. Stay calm.
Arrange a further appointment with somebody in the near future.
Offer availability.
Discussion
Whilst this station is primarily an assessment of communication skills,
the examiners may reasonably be interested in your understanding
of the basic principles of the management of lung cancer. Lobectomy
and pneumonectomy are used for non-small cell carcinoma, and can
prolong life, improve quality of life and relieve pain. Adenocarcinoma
is the most common non-small cell cancer, when tend to develop to
the periphery. They tend to metastasize to the bone, CNS, adrenal
glands, liver and opposite lung. Squamous cell carcinomas tend to be
located in the more central part of the lung. Small cell carcinoma is
the most aggressive type of cancer and has the worst prognosis.
Radiotherapy and chemotherapy is the primary treatment for small
cell carcinomas. Contraindications to surgery in non-small cell lung
cancer include: Metastatic carcinoma, transfer factor < 50%, severe
pulmonary hypertension, uncontrolled cardiac arrhythmias, poor lung
function, left laryngeal nerve palsy, malignant effusion, dysphagia,
mediastinal lymph node involvement, superior vena cava obstruction,
phrenic nerve palsy, rib or distant metastasis.
The examiners may wish to discuss related oncology issues, such
as the importance of oncology patients entering multicentre clinical
research trials. It may be useful to be aware of documents such as the
Calman-Hine report which was produced in response to concerns
about variations in treatment around the country. This report
recommends that cancer services should be organised at three levels.

Primary care is seen as the focus of care; the commoner cancers will
be treated in Cancer Units in local hospitals which have the expertise
and facilities to support a multidisciplinary team; and the less common
cancers will be treated in Cancer Centres situated in larger hospitals,
which will also support Cancer Units by providing specialist services
such as radiotherapy.
ALZHEIMERS DISEASE
Scenario 4
Problem: Breaking bad news (a diagnosis of Alzheimers disease).
Patient name: Peter Matthews (aged 64).
Peter Matthews is a 64-year-old man who presented with increasing
memory difficulties. He himself reported an incident where he went
to his local corner shop, but on arrival forgot what he had intended
to purchase. Overall, he feels that his mood has been fine, and he
reports that he has had no other difficulty. In light of this symptom,
his GP arranged a CT head scan which demonstrates cerebral atrophy.
Neuropsychology confirmed short-term memory problems. You are
the FY2/ST1 for Neurology and General Medicine, and you are to
see Peter Matthews in outpatients regarding his investigations. The
multidisciplinary memory clinic team have discussed Mr. Matthews,
and they feel that the most diagnosis is Alzheimers disease.
Explore the patients understanding of the condition and
expectations/suspicions of what may be wrong.
Discover what the patient understood about the tests (e.g. CT
scan demonstrating cerebral atrophy). Explain that there is no
single test for this particular condition, although results may be
supportive of such a condition.
Explain that the disease tends to be a slowly progressive disease,
but the rate of progression can be unpredictable. The disease is
characterised in its early stages by loss of memory. I can see how
hard your memory loss has been to deal with.
He should aim to optimise general health, and should use cognitive
aids (e.g. clear labelling diary). Current medications include
donepezil, a cholinesterase inhibitor, for mild dementia. Main side
effects are cholinergic. It is a case of taking things as they happen.
Explain that lifestyle changes can be helpful (for example, locking
up any rooms in the house that are not in use, locking up any
drawers that contain important documents).
225
The patient may wish to know whether the condition runs in

families. Alzheimers disease where there is a family link is called
familial Alzheimers disease, and is more common among younger
people (under the age of 65). Research has shown that even for
people with a strong family history of early onset Alzheimers
disease, only 50% of cases are caused by a genetic defect. Some
cases of Alzheimers disease in people under 65 are, however,
inherited. On average, half of the children of a person with one of
these rare genetic defects inherits the disease. Probably all those
who inherit the genetic defect develop Alzheimers disease at a
comparatively early age.
Tell him about the support offered by the Alzheimers Disease
Society. Mention that benefits are available to patients with
Alzheimers disease, and their carers, and these can be ascertained
from the Citizens Advice Bureau.
Explain that daycare may be available for the patient, giving respite
for the carer.
Ask her if he has any questions. Offer an appropriate time for
follow up.
TESTICULAR CANCER
Scenario 5
Problem: Breaking bad news (A diagnosis of testicular cancer).
Patient name: William Charles (aged 21).
William Charles is a 21-year-old man saw his GP because of a lump in
his testes. A nurse had accidentally done a pregnancy test which was
positive. However, he was unaware this had been done, and had just
been told that a urine sample was needed to look for infection. A CT
scan, with subsequent biopsy, arranged by his GP, demonstrates a
testicular tumour. He has a girlfriend of two years, to whom he is
close. You are the FY2/ST1 for General Medicine. He has attended
clinic to discuss the result.
Explore the history of how the patient realised that something
was wrong. Once the patients understanding of the condition has
been established, it may be possible to predict if he is expecting a
diagnosis of cancer. If he is aware that cancer is a possibility, the
patient should be informed of the diagnosis in a clear and
sympathetic manner. He may wish to see his CT scans or the
histology report, which is sometimes useful.

Explain the nature of the disease, the need for cyclical combination
therapy over a period of several weeks, and its side-effects. Explain
that the treatment will give him a very good outcome. If the patient
has not considered cancer as a possible diagnosis, the patient should
ideally be given small pieces of information at a time, working
towards the diagnosis. The doctor should be relatively positive,
as the outcome is usually good with chemotherapy.
Allow the patient time to react to the diagnosis and pause.
He may ask why the urine sample was taken. The author of this
scenario would like you to consider what ethically you would do
in this scenario.
Explain the need for subsequent cytotoxic chemotherapy: Logistics
(when and where) and side-effects (e.g. infection, alopecia, nausea
and infertility).
Explain the implications of the treatment of his condition: Cosmetic
testicular prostheses can be inserted; fertilityunaffected by
previous surgery, likely to be infertile after chemotherapy, but
semen can be frozen and stored; need for future monitoring of
response to treatment: CT body and blood tests. He may wish to
discuss these findings in light of his personal circumstances (such
as his girlfriend).
Emphasise the very good prognosis for testicular cancer: Around
90% cure. Ask the patient if he understands what has been said.
Summarise the consultation and ask if he has any questions.
Arrange medical follow-up. Arrange a point of contact with the
oncology nurse specialist. Make sure that there is someone he can
talk to, or someone at home with him.
HODGKINS DISEASE
Scenario 6
Problem: Breaking bad news (Hodgkins disease).
Patient name: Claire Barron (aged 27).
Claire Barron aged 27 presented to her GP feeling unwell a month
ago with fever and loss of appetite. A chest X-ray in the clinic showed
bilateral hilar lymphadenopathy. The consultant did not discuss the
diagnostic possibilities but arranged for a mediastinal biopsy
(mediastinoscopy) which was performed by a thoracic surgeon 2
weeks ago. You are the FY2/ST1 for a firm that specializes in
haematology and oncology. Your Consultant is away today, and Miss
Barron has come back for the biopsy result. Unfortunately, this result
states Hodgkins disease as the diagnosis.
227

Explore the patients understanding of her symptoms and
expectations/suspicions of what may be wrong.
Ask her if she has heard of Hodgkins disease.
Explain that Hodgkins disease is a malignant proliferation of a
certain type of cells which are involved in the immune system and
called lymphoid cells. Prognosis depends upon sampling these in
biopsy.
The symptoms should be explained to the patient. Patients usually
present with enlarged, painless nodes, and 25% have constitutional
upset, e.g. fever, weight loss, night sweats, pruritus, and lethargy.
Explain that there are doctors who specialize in this disease and
that there are well-established treatments available. The tests which
need to be done should be explained, including lymph node biopsy,
blood tests, CT/MRI thorax, abdomen and pelvis.
Tell her that you will refer her urgently to the clinical oncologist
for further staging, which confers a treatment plan and prognosis.
Explain the options for treatment: radiotherapy is for stages IA
and IIB, chemotherapy for IIA with >3 areas involved to IVB.
Complications of treatment include hypothyroidism, lung fibrosis,
nausea, alopecia, infertility, infection and secondary malignancies.
Ascertain how much the patient has taken in regarding the
information.
Avoid giving specific times regarding prognosis, and provide hope.
Ask who is at home to support her. It is wise to inform the GP
straight away for primary care support. Check that she is not
driving home on her own.
Offer an appropriate for follow-up.
Discussion
The prognosis of Hodgkins disease depends on the histological type
of disease. Lymphocyte-depleted has a poor prognosis, the others
have good prognosis (nodular sclerosing, mixed cellularity,
lymphocyte rich). It also depends on the staging of disease. The
examiners may expect some understanding of the staging of disease.
Stage I is confined to a singly lymph node region, II involves two or
more regions on the same side of the diaphragm, III involves nodes
on both sides of the diaphragm, and IV involves spread beyond the
lymph nodes.
Recurrence of Breast Cancer

Breaking the bad news of a recurrence of breast cancer is a particular
example of a bad news scenario, but there are features of this scenario
which reflect that palliative care is a speciality where patients can lose
hope. It is therefore essential to elicit a patients own specific fears,
before addressing them.
Consider the understanding of illness, the expectations and
concerns about the future.
Consider the effect of the illness physically and emotionally.
Provide medical reassurance (their symptoms will be identified
promptly, controlled as far as possible and that they will remain
comfortable).
Explore the social support (in terms of Doctors, Nurses, Church
etc.)
Explore thoughts and fears about the future, dying, worries, plans
made, plans not made.
Explore how the family is coping with the illness.
Scenario 7
Problem: Recurrence of breast cancer.
Patient name: Anna Fine (aged 48).
You are the FY2/ST1 on the medical ward to which Mrs. Fine, a 48years-old lady, who was admitted a month ago with acute confusion
secondary to mild hyponatraemia and severe hypercalcaemia. She
was treated with intravenous fluids and pamidronate, and was then
well orientated and lucid. She had a mastectomy for breast cancer 12
years ago followed by radiotherapy but no chemotherapy. She was
last seen only 6 months ago in breast clinic, and reassured that
everything was going well. She even underwent a mammogram at
that stage, reported as normal. She had been otherwise well on this
admission, until she began to complain of increasing back and sacral
pain. The House Officer requested X-rays which demonstrated changes
consistent with bone metastases, confirmed on a later DEXA bone
scan. Her chest X-ray also demonstrates a moderate effusion and
cytology confirming malignant cells. Your task is to explain to Mrs.
Fine that she has advanced metastatic cancer, and will be referred to
the oncology team for further care that is likely to include
chemotherapy and radiotherapy.
229
Explore the patients understanding of the condition and

expectations/suspicions of what may be wrong. Explore the
understanding of her prognosis: She may have been convinced
that she has been completely cured of cancer, but her recent
admission cast may have doubt upon this.
Explain the meaning of the tests and results (e.g. bone scan), and
explain that the cancer has spread.
Be prepared for the patients response. She may demonstrate
denial, before being angry towards the initial therapy given. The
candidate should not criticise previous treatment, and even if he
is not able to understand the logic of the initial therapy, he should
still find some way of reassuring the patient about the
appropriateness of initial therapy.
Explain that it is difficult to predict what course the disease will
take. However, prompt investigation of the cause of symptoms,
and treatment for these symptoms and side-effects can be given.
Inform the patient that you will comply with her wishes. Explain
that you will listen to the patients concerns and involve her in
decision-making.
Explain that her symptoms will be treated, but that the treatments
have side effects, for example chemotherapy can cause nausea and
vomiting, diarrhoea and constipation. The best treatment may
involve radiotherapy, chemotherapy or hormome therapy, either
given alone or in any combination or order. Explain that the
treatment will shrink the cancerous growths but it may be
impossible to get rid of the cancer completely. Some patients go
into complete clinical remission. The candidate should be prepared
to discuss the pros and cons of an optimistic versus a pessimistic
approach in discussion.
Outline that breast cancer treatment is carried out by different
specialists who work together as a team, including psychologists,
physiotherapists and also members of the appropriate religion.
There are a number of sources of professional support. It is
impossible to predict who will do well until the treatment is
underway. The GP has responsibility for health care, and the
District nurse can provide nursing care and organise for equipment.
Macmillan nurses are available, who are specialists in pain and
symptom control for people with cancer, and emotional and
psychological support for carers. Palliative Care Teams have
expertise in symptom control and support for patients and their
carers. A social worker can assess what welfare benefits a patient

may be entitled to. They can arrange social services and other
practical help. Explain that there are organisations such as Cancer
BACUP can help, and these organisations usually have their own
websites on the internet.
Enquire further about any further expectations (for example, she
may have booked a holiday abroad, in which case you would need
to inform her about the possible need for assessment for a fitness
to fly, and what local arrangements could be made at the place
that she is flying to regarding local therapy for emergency such as
cord compression).
It is important to maintain a positive and optimistic outlook. Ask
the patent if he has told other members of the family, or if he
would like them to know of his decision. Ask if he has sorted
things out at home. Is there any one else who would like to be
contacted? Explore the patients understanding of what refusal
will entail. A good candidate should be able to agree a summary
and plan of action with the subject. Summarise what has been
discussed. Ask if he has any questions. Make appropriate followup arrangements.
At some later date (guided by the scenario), it may be important
to discuss resuscitation status.
Giving information: Explaining diagnosis, treatment and prognosis to
competent patients.
Several scenarios used in this station involve simply explaining a
diagnosis or treatment to competent patients. A definition of
competence is provided in the next section C, and is not the focus of
this section. A recent study by Kindelan and Kent (1987) in British
general practice showed that patients placed the highest value on
giving information about diagnosis, prognosis and causation of their
condition. Doctors however greatly tend to underestimate their
patients desire for information about prognosis and causation, and
overestimated their desire for information concerning treatment and
drug therapy. Patients individual information needs were not elicited.
You should explore the patients perception of their condition and
prepare them. Consider What have you been told about your condition?
Find out what the patient wishes to know. Bear in mind that patients
are often extremely well informed, and therefore if a patient presents
with a condition that you may in actual fact know not that much
about, for example alpha-thalassaemia trait, listen to the patient! You
should show you are listening through body language, and encourage
the patient to tell their story too.
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Do not forget that some scenarios will deliberately go beyond the

scope of a junior doctor in a medical firms professional experience or
authority (e.g. a certain condition in a pregnant lady). In such cases,
you will be expected to recognise the need to refer the matter.
Examples of suitable scenarios for this station include:
Giving Information About Diagnoses

This will not be a test of your knowledge of particular medical
conditions, but rather an approach of how you impart information
about these particular diagnoses. Some useful points to consider are:
1. Information must be related not only to the facts, but also the
patients ideas about the condition. Have you heard of this condition
before?, Have you any ideas about this condition?, or What have you
been told about this condition?
2. Use a logical sequence to explain the cause and effect of the
condition in the context of the patients symptoms (why it occurs,
possible clinical problems, the likely natural history with/without
treatment).
3. Be alert to beliefs, concerns and expectations. Establishing prior
experience can help you understand any specific fears that may
relate to it.
4. Tell one thing at a time and check the patient understands before
moving onto the next.
5. Use simple language; translate any unavoidable medical terms and
write them down.
6. Make your information direct. Repeat important information.
7. At the outset, show patients that you will write down the key
words, use a simple diagram, and offer them aids to memory.
8. Acknowledge the possible need for further referral in diagnosis
or management.
9. Encourage feedback, invite questions and check understanding.
Be prepared to admit uncertainty if the patient asks you something
you cannot answer.
A NEWLY DIAGNOSED DIABETIC

Scenario 8
Problem: Giving information (a new diagnosis of diabetes mellitus).
Patient name: Tim Scott (aged 19).
Tim Scott is a 19-year-old man who was referred to endocrinology
outpatients after his fasting blood sugar was found to be elevated.

He had noticed some transient blurring of vision, which has
subsequently thought to be due to osmotic changes in the lens as a
result of blood sugar problems. His glucose tolerance test supported
the diagnosis of diabetes mellitus. Please discuss with him.
Introduce yourself to the patient and establish rapport. Establish
the patients understanding of his symptoms and their implication
(e.g. You say that you have been passing water frequently, and felt thirsty.
Have you had any thoughts about what these symptoms might be due
to?), and expectations.
Ask the patient whether he has had any experience of diabetes in
other people (e.g. his father may have had diabetes and developed
complications from that), and respond empathetically.
Explain to the patient the basic mechanisms underlying the diabetes
mellitus. You should then ask the patient if he would like any
other information (e.g. Would you like to know about the tests I would
like to do to confirm the diagnosis and the stage of your diabetes?).
Explain the aims of treatment to reduce the risk of complications:
macrovascular (IHD, cerebrovascular and peripheral vascular
disease) and microvascular (nephropathy, retinopathy and
neuropathy). All of these can be reduced with optimal glycaemic
control, but other important risk factors are smoking, alcohol excess,
hypertension, hyperlipidaemia, and obesity.
Emphasise the need for lifelong treatment.
Explain the multidisciplinary approach: Diabetic specialist nurse,
dietitician, chiropodist, ophthalmologist, and need for teamwork.
Outline possible treatments: emphasise that dietary modification
is a most important aspect of treatment, combined with exercise.
Discuss the possibility of oral medication, if this is unsuccessful.
Discuss the possibility of insulin therapy in the future. Address
other risk factors, i.e. hypertension, hyperlipidaemia, smoking.
Emphasise the need for compliance and regular review. Introduce
him to the diabetic team.
Point the patient in the direction of further information about
diabetes. Arrange patient education sessions. State clearly that he
will require follow-up for review of his diabetes to detect and
treat any complications.
It is important that you check the patients understanding by asking,
Can you now tell me what you understand about what I have explained
to you in terms of the tests needed, the extent to which we should be able to
control your illness, and the likely treatment?
Arrange appropriate follow-up with the multidisciplinary team.
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THYROTOXICOSIS
Scenario 9
Problem: Giving information (a new diagnosis of thyrotoxicosis)
Patient name: Annabel Smith (aged 29)
Annabel Smith is a 29-year-old lady who has lost 2 kg over the last
few months, despite a good appetite and intake of food. She has
become somewhat irritable at work, and slightly tremulous in both
her hands which she thought was due to her anxiety. Blood tests
confirms that she is hyperthyroid. Examination, apart from the tremor,
is normal. Her pulse is 90, regular. You are the FY2/ST1 for
Endocrinology. She has returned to clinic for the results of her blood
tests.
Introduce yourself and establish rapport.
Explore her knowledge of the symptoms, and what they possibly
meant. Ask what she understood by the need for the blood test.
Explain the results of the blood test.
Explain the nature of an overactive thyroid and the pathological
consequences of an untreated disease. This might focus on current
symptoms. When considering loss of weight, confirm that this
weight is lost despite a good appetite and eating vast amounts.
Advise about some of the manifestations of thyrotoxicosis can take,
e.g. skin (warm and sweaty due to vasodilatation), cardiovascular
(tachycardia, with increased cardiac output due to increased
peripheral oxygen utilisation and increased cardiac contractility,
atrial fibrillation, mitral valve prolapse), ocular, gastrointestinal
(weight loss due to increased basal metabolic rare, increased gut
motility with associated diarrhoea and malabsorption), locomotor,
neurological (emotional lability, insomnia, irritability, anxiety,
proximal muscle weakness, tremor) and reproductive system.
If a smoker, the patient is at greater risk of eye disease, and so
therefore should be asked if there is any noticeable bulging of the
eyes or double vision. Discuss the treatment options.
Explain that her symptoms will resolve with treatment, but may
take months to resolve completely. For medical therapy, warn of
the potential side-effects, especially agranulocytosis. Thus, must
be given both verbally and in writing. Establish her last menstrual
period, wishes for pregnancy and if she has any children.
Establish the need for regular review.
Point the patient in the direction of further information about
thyroid disease. Arrange patient education sessions.

It is important again that you check the patients understanding
by asking, Can you now tell me what you understand about what I have
explained to you in terms of the tests needed, the extent to which we should
be able to control your illness, and the likely treatment?.
Giving Information About Treatments

Encouraging a patient to adopt a treatment requires that the patient
understands the risks and benefits of that treatment, and it is necessary
before consent for a treatment can be acquired. For any procedure,
treatment or operation, the doctor needs to explain the nature of the
procedure. The doctor must exercise sensitivity to patients fears, and
it is a legal requirement to inform the patient of risks, benefits and
alternative treatments which demonstrate both good practice and
avoidance of negligence. Doctors may be faced with litigation when
patients understand the benefits of the treatment, but do not
understand the risks of the procedures that they are undergoing. The
duty of the doctor is to provide this information frankly to the patient.
The nature by which consent is obtained is not only fundamental to
the doctor/patient relationship, but is also a key way to which patient
autonomy is respected. In order to obtain consent, the doctor discloses
information to a patient who is legally competent. A sensible approach
in which to do this is suggested below:
1. Explain the reasons for considering the treatment (Is the treatment
critical, essential, elective or discretionary).
2. Give the patient a chance to react to the need for treatment.
3. Consider whether there are any likely benefits of treatment
according to currently accepted medical practice, but be aware
of overwhelming patients with outcomes of studies.
4. Explain what the treatment will need for the patient in terms of
the frequency of dosing, the duration of therapy, any special
instructions, how long the treatment will take.
5. Any requirement for any specific monitoring, e.g. blood
monitoring.
6. The common, as well as uncommon, side effects and any
discomfort of treatment.
7. Suggest any alternative to treatment. You should be offering
suport, i.e. making supportive statements but also giving practical
advice such as details of counselling services and appropriate
literature.
8. How soon knowledge about the effects of the proposed
intervention will be made available.
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9. Give ample opportunity for questions.

10. Keep it short and simple.
11. Finally seek consent. Remember that you are explaining the reason
for a treatment and not telling your patient that they must have
it. Following your explanation, you should seek informed consent
to proceed.
12. For negotiating a management plan, clarify the task, explore
concerns and explanations, keep to a framework, share
management options It might help if, I wonder if etc.
13. Show respect for the patients autonomy; do not behave
coercively.
14. Invite the patient to ask any questions.
Studies have consistently shown that between 10 and 90% of
patients prescribed drugs by their doctors (with an average of 50%)
do not take their medication at all or take it incorrectly. Walton et al
(1980) estimated the cost of wasted drugs per year in the UK is of the
order of 300 million. In the scenario, you should specifically ask how
the patient is with regard to symptoms. Ask any patient who appears
not to be compliant with his medical regimen whether he has not
been taking his medication, and, if so, enquire why, e.g. side-effects,
forgetfulness, inability to get hold of the tablets, poor information
about how to get the tablets, the purpose of taking the mediction,
unpleasant side-effects. Consider alternative simplified drug regimens.
Consider arranging with the health visitor and your Consultant
directly observed therapy where ingestion of every dose is witnessed.
Patient recall is increased by categorisation, signposting, summarising,
repetition, clarity and use of diagrams (Ley, 1988).
HORMONE REPLACEMENT THERAPY (HRT)

Scenario 10
Problem: Commencing treatment (hormone replacement therapy)
Patient name: Laura Wood (aged 57)
Laura Wood is a 57-year-old lady who has been experiencing the
symptoms of the menopause. She has read about HRT, and has
considered it as a treatment for her troubling symptoms. You are the
FY2/ST1 for General Medicine. Please discuss with her HRT as an
option, and advise accordingly.
Introduce yourself to the patient.
Establish the patients perception of her symptoms.
Explain the concept of HRT and explore the patients beliefs and
concerns about it. Establish then the patientss expectations.

Explain the potential benefits: HRT is an effective means of
controlling the vasomotor and genital symptoms associated with
the menopause. It prevents osteoporosis. There is a possible
decrease in the risk of ischaemic heart disease, but the evidence is
unlear. It decreases the risk of uterine carcinoma and possibly
colonic carcinoma.
Explain the likely course of treatment, and related issues. Current
recommendations are to stop HRT after 5-10 years of treatment,
although the increased risk of breast cancer attributable to HRT is
not thought to begin until around 50 years of age. Oestrogen-only
HRT tablets or patches may be used in hysterectomized patients,
but preparations associated with progesterone should otherwise
be used to limit endometrial hyperplasia and the risk of endometrial
malignancy. Amenorrhoea need not be awaited before starting
HRT. Cyclical (sequential) hormone regimens are generally used
in perimenopausal women and continuous combined regimens in
postmenopausal women. Continuous combined treatment is
associated with a high risk of irregular bleeding in perimenopausal
women but should not cause induced bleeding in postmenopausal
women. Postmenopausal bleeding generally necessitates
investigation to exclude endometrial malignancy.
Describe briefly the evidence concerning the risks associated with
hormone replacement therapy. HRT increases the relative risk of
venous thromboembolism, but again the absolute risk is low, and
possibly offset by the favourable effects of HRT on lipid profiles
and potential cardiovascular benefit. Studies are inconclusive as
to whether HRT induces (or even increases) cardiovascular risk.
There is no current evidence to support the use of HRT in either
the primary or secondary prevention of coronary heart disease,
and no evidence that HRT reduces stroke risk. A systematic review
and meta-analysis has suggested that HRT may have a role in
reducing dementia and cognitive decline. HRT does not cause
weight gain. Discuss alternatives to HRT, e.g. clonidine for hot
flushes, evening primrose oil, topical oestrogens.
Explain the need for annual mammograms and self-examination.
Explain that HRT will result in her continuing to have regular
withdrawal bleeds that she may find troublesome. Ultimately the
decision is the patients, and she needs to weigh up the theoretical
risks and inconvenience against her troublesome symptoms. Ensure
that she understands all the issues. Finally ask if she has any
questions.
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WARFARIN
Scenario 11
Problem: Commencing treatment (warfarin)
Patient name: Jennifer Salmon (aged 34)
Jennifer Salmon is a 34-year-old lady who has recently undergo a
mitral valve replacement. She was diagnosed both clinically and
echocardiographically with severe mitral stenosis. She is about to be
discharged having undergone the replacement, but your Consultant
would like you to discuss with her the need for anticoagulation with
warfarin. She has made it known to the senior CCU nurses that she
and her husband had been wishing to try for a family by the end of
the year. You are the FY2/ST1 for Cardiology. Please discuss with
her the need for warfarin treatment, and any concerns she may have.
Introduce yourself and establish rapport. Explore the patients
perception of her condition, and what she has been told about it in
the past. Ask about her beliefs, concerns and expectations of her
valve replacement.
Ascertain what she knows about aspects of the treatment plan,
including knowledge of warfarin.
Some people only have heard of warfarin in the context of rat
poison. Explain that blood clots normally form to stop bleeding
that has occurred as a result of injury to the tissues. Explain that
the clotting process is complicated, but sometimes a blood clot can
form abnormally within blood vessels and dislodge such that blood
supply to a vital organ such as the heart, brain or lungs is impeded
(thromboembolism).
State that loading with warfarin is necessary, and explain what
this involves.
Consider the need for treatment and the precautions needed. It is
used for abnormal blood clots in conditions with increased risk
(e.g. prosthetic heart valves, atrial fibrillation), and prevention of
PEs and DVTS. Consider all the drug history and lifestyle factors
that would impact upon taking warfarin, i.e. the patient should be
warned to take extra care when participating in physical activities
because minor injury can result in bleeding. Also, warfarin inhibits
vitamin K, therefore eating large amounts of green vegetables can
reduce the effect of warfarin and should be avoided. Large amounts
of alcohol can also increase the effect of warfarin.
The candidate should be able to give adequate information to the
patient about how to take the treatment and what precautions to
observe, in terms suitable for a patient to understand. If there is

any bruising, bleeding, dark stools, dark urine, or fever, then a
Doctor should be seen.
Warn about common side effects including easy bruising, rash,
jaundice, alopecia, skin necrosis, liver disorders, pancreatitis and
nause and vomiting. OCP and rifampicin can reduce the effect of
warfarin.
The need to monitor the INR should be explained, as too much
anti-coagulation can adversely increase the risk of bleeding. If there
are any problems with ongoing bleeding, the patient should seek
medical attention immediately. Warfarin is the long-term
anticoagulant of choice in non-pregnant patients, but its great
disadvantage in pregnancy is that it freely crosses the placental
barrier because of its low molecular weight and can harm the fetus.
Explain the need to carry an anticoagulation book, and the need
to tell the dentist/other doctors about treatment.
Ask for any further questions, and make appropriate follow-up
arrangements.
Discussion
The anticoagulant effect of warfarin is mediated by inhibition of the
vitamin K-dependent gamma-carboxylation of coagulation factors II,
VII, IX and X and proteins C and S. The laboratory test most commonly
used to measure the effects of warfarin is the prothromnin time.
Loading is necessary because, in the first few days, factor VII is
depressed, but five days are needed before factors II, IX and X are
suppressed.
Adverse fetal effects from warfarin may result from the
teratogenicity of the drug and its propensity to cause bleeding in the
fetus. Warfarin should also not be used in pregnancy, peptic ulcer or
uncontrolled high blood pressure. Difficult decisions arise when
patients are on long-term warfarin therapy because of prosthetic valves
or recurrent pulmonary embolism become pregant. Any changeover
to low molecular weight heparins (LMWH) must be carried out with
care and under the multidisciplinary care of the obstetrician and the
haematologist. Warfarin crosses the placenta with a risk of placental
or fetal haemorrhage. Warfarin therapy is contraindicated in the first
trimester because of its association with fetal epiphyseal haemorrhage.
In the second and third trimesters, warfarin may cause fetal atrophy,
microcephaly, optic atrophy, spasticity, and mental retardation.
However, warfarin is safe during breastfeeding. In the initial
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treatment of a DVT, LMWH which does not cross the placenta may
be administered subcutaneously according to body weight. LMWH
is not contraindicated in breast-feeding women.
STATINS
Scenario 12
Problem: Commencing treatment (a statin)
Patient name: Luke Dunn (aged 48)
Luke Dunn is a 48-year-old who, despite a good BMI, has a
consistently high cholesterol. He had an uncomplicated myocardial
infarction 4 years ago, but made an excellent recovery. Recent
investigations showed: plasma cholesterol 7.2 mmol/l, LDL-cholesterol
4.9 mmol/l, HDL-cholesterol 1.1 mmol/l and triglycerides 1.4 mmol/
l. He is a life-long non-smoker, and his diet has been good. Despite
dietary advice, his cholesterol remained high. You are the FY2/ST1
for General Medicine in clinic. Please discuss with him the possibility
of commencing the statin simvastatin.
Explore his knowledge of his condition, and the relevance of
cholesterol. Explore briefly relevant risk factors: i.e. cardiovascular
history, diabetes history, hypertension history, family history of
ischaemic heart disease, alcohol, smoking, dietary and exercise
history, concerns of patient.
Explain the need for reducing cholesterol in terms of the future,
e.g. heart attacks, stroke. There is bad cholesterol (LDL) and
good cholesterol (HDL). Simvastatin decreases the production
of LDL cholesterol (and total cholesterol) by competitively blocking
the action of the enzyme in the liver that is responsible for its
synthesis (HMG-CoA reductase).
Explain that, as the body produces most cholesterol at night, statins
are generally more effective at night.
Explain the likely benefits of the therapy (cause regression of
coronary atheromatous plaques, may ameliorate peripheral vascular
as well as coronary artery disease, slightly reduce the risk of
stroke), and explain what the treatment will mean for the patient
in terms of frequency of dosing, the duration of therapy, any special
instructions (e.g. the tablet should be taken with meals), any
requirements for blood monitoring.
Advise that excessive amounts of alcohol should not be taken, and
grapefruit juice should ideally be avoided in excess because it can
increase the amount of medicine in the blood.

The patient should see the doctor if there is pain or tenderness in
the muscles, particularly if accompanied by symptoms of generally
feeling unwell. Blood tests should be monitored before treatment
(e.g. LFTs), and during it. It should be used with caution in the
elderly and in patients with hypothyroidism, or history of liver
disease. It should not be used in pregnancy.
Explain the side effects which are common or serious, and explain
how the side effects weigh up against the benefits. These side
effects are abdominal pain, constipation, flatulence, headache,
dizziness, pins and needles, indigestion, nausea and vomiting,
anaemia, liver disorders, hair loss and muscle disorders.
Common medications that increase side effects are amiodarone,
verapamil, diltiazem, itraconazole, and erythromycin. Explain what
should be done when a side effect occurs.
Give ample opportunity to react to the information, and ask for
questions. Seek consent to proceed. Explain that other health
professionals may be involved, such as dietitians. Arrange
appropriate further information if necessary, and follow-up.
STEROIDS
Scenario 13
Problem: Commencing treatment (steroids for rheumatoid disease)
Patient name: Sarah Collins (aged 37)
You are the Rheumatology FY2/ST1 in clinic in outpatients. You have
just discussed the case of Mrs. Collins, a 37-year-old woman, with
your consultant who feels that she should start steroids. She has had
rheumatoid disease for three years. So far, her main symptoms have
been stiff hands, and she required NSAIDs to control her symptoms.
However, over the last few months, she has worsening disease, and
your team decision is that she should start prednisolone 30 mg od to
control her symptoms. Please discuss with her.
Polite introduction and establish rapport.
Establish the patients understanding of her disease and the need
for steroids.
Try to get some feel of the impact of the disease on her life,
including the use of her hands (eating, washing) and other aspects
of a routine functional assessment (for example, managing stairs,
using a telephone, cooking, shopping).
Explain that corticosteroids are hormones produced naturally by
the adrenal glands which have important functions including the
241
control of inflammatory responses. Explain that prednisolone is a

synthetic corticosteroid that is used to increase inflammation in
various diseases.
Explain the need for steroids to prevent attacks and the
consequences of poorly controlled disease. Explain that steroids
should be taken after food. A steroid card will be needed if
prednisolone taken for more than 3 weeks, which contains details
of prescriber, the type of steroid, dose taken and duration of
treatment. There will also be a need for medic alert bracelet and a
hydrocortisone pack (for parenteral self-administration if shes
unable to take oral medication). If there is any illness, trauma or
surgery, the steroid dose may need to be temporarily increased.
A good candidate should be able to explore the impact of disease
on the patients daily activities and quality of life, and explain the
need for further treatment and advantages of using steroids.
Warn that the steroids should also not stopped suddenly, as longterm use suppresses the natural production of steroids by the
adrenal glands. She should therefore not miss a dose. There may
be increased susceptibility to infections.
Common side-effects are difficulty in sleeping, depression, skin
thinning, weight gain, irregular menstrual cycle, osteoporosis,
diabetes, acne, increased susceptibility to infection, high blood
pressure.
Your role in discussing the adverse effects should not be confined
to reeling off a long list of adverse effects but rather to have a
balanced discussion. Remember you are automatically making (or
should be making) risk-benefit calculations in your everyday jobs
when considering investigations and treatments.
She may mention weight gain. You can say, Yes, these steroids can
cause weight gain and they do this not only by causing the retention
of fluid but also by increasing appetite. So knowing this you can
plan ahead and try to eat more sensibly with smaller portion sizes
(although offer her a dietitian appointment to help her plan the
strategy more effectively). She could also exercise more frequently.
By saying this, you are offering back some control of the situation.
She might have heard that steroids will thin her bones. Again explain
that this is a possibility but that as a young person she is likely to
have strong bones to begin with. Reassure her that you will be
ordering a (DEXA) scan that will monitor her bone strength.
Explain that there are effective treatments she can take that will
prevent bone loss and that exercise can also help.

What about the blood pressure doctor?. Steroids tend to cause
retention of water and this may cause an increase in blood pressure.
Reassure that regular measurements of blood pressure can be taken,
and that treatments are available to counter the rise in blood
pressure.
What about the blood sugar doctor?. Corticosteroids do not
precipitate high blood glucose (say sugar instead of glucose) in
everyone who takes the tablets. Some people are more susceptible
especially if there is a family history of diabetes and if they are
overweight. Again, there are effective ways of monitoring for this
and treating if ncessary.
State that these will be minimised by ensuring her dose is tailored
to her condition. Osteoporosis can be minimised by concomitant
bisphosphonate therapy. The effects of steroids are reduced by
antiepileptics, rifampicin, barbiturates and aminoglutethimide.
When taken with NSAIDs, there is an increased effect of adverse
effects on the gut. Ensure that the patient understands what has
been said and ask if she has any questions.
It is very important to ask the occupation of the patient in certain
situations. If you are not given this information, it is a good idea
to ask. If the person has never had chickenpox, close personal
contact should be avoided. If exposed, the patient should see his/
her doctor urgently, as these diseases can be threatening. This
would be especially important if, for example, she was working as
a nanny.
Summarise what has been discussed. Arrange appropriate followup.
SURGICAL TREATMENTS FOR MEDICAL DISORDERS

Benefit and risk of a CABG in a patient with triple vessel disease.
Scenario 14
Problem: Proposing treatment (coronary artery bypass graft)
Patient name: Andrew Foster (aged 53)
Andrew Foster, a 53-year-old man, was admitted with his third
episode of chest pain at rest this year. This pain was cardiac sounding
in history, and the ECG demonstrated dynamic changes. His troponin
was elevated 12 hours after the onset of the pain. A coronary
angiogram was arranged on this admission, which demonstrated
243
multiple narrowings in the coronary circulation. He had hoped that

these vessels would be amenable to stenting, but the Cardiology
Consultant on review of the angiogram data feels that he ought to be
referred to Cardiac Surgery. You are the FY2/ST1 for Cardiology.
Please discuss the possibility of coronary artery bypass grafting as an
option for him.
Introduce yourself and establish good rapport.
Establish the patients beliefs and concerns of understanding the
disease, its severity and likely expectations. Ask about smoking
behaviour, but avoid being judgemental about his smoking.
Explain the results of the recent angiogram. Establish the patients
understanding and expectations of possible treatment options.
Explain the need for the procedure, e.g. none of the vessels are
amenable to stenting.
Explain that coronary artery bypass graft (CABG) surgery,
sometimes just called bypass, is the procedure that enables a
blocked area of the coronary artery to be bypassed so that blood
flow is not hindered. During bypass surgery, a healthy artery or
vein is taken from the leg, arm or chest and transferred to the
outside of the heart. The new healthy artery or vein then carries
the oxygenated blood around the blockage in the coronary artery.
Explain why CABG surgery is performed, i.e. to relieve symptoms
of coronary artery disease, reduce the possibility of more heart
problems, and to prolong life.
As with seeking consent for any procedure, explain explicitly that
there are complications and risks associated with CABG
procedures. Complications associated with coronary artery bypass
grafting may include stroke, damage to the aorta, the potential
damaging effect of emboli, bleeding, vein graft occlusion or
stenosis, arrhythmias, acute myocardial infarction, angina, or death.
After the procedure, the patient spends 5-7 days in hospital. After
a day in the ICU, the patient normally moves to a hospital wound,
and the incision heals. Recovery from any surgery varies for each
patient. Most patients start feeling better within 4-6 weeks. It is
important in the post-operative phase to follow doctors
instructions and to report any problems (abnormal pain, signs of
infection) immediately.
Arrange for the patient to meet the surgical team, and arrange
appropriate follow-up.
RENAL TRANSPLANT
Scenario 15
Problem: Proposing treatment (renal transplant)
Patient name: Elaine Cook (aged 58)
Elaine Cook is a 58-year-old lady who has polycystic kidney disease.
Four years ago, she commenced continuous ambulatory peritoneal
dialysis, but her renal function has remained poor. She now has endstage renal failure, and requires further support. Haemodialysis has
previously failed. You are the renal SHO. Mrs. Cook would like to
discuss with you the possibility of a renal transplant, and what
practicalities will be involved.
Introduce yourself to the patient and establish rapport.
Explain the patients understanding of the condition requiring renal
transplant. A candidate should be able to explain to the patient
that the kidneys are not working and why. They should be able to
explain the significance of this and what would happen if left
untreated. This should be done in an empathetic manner in terms
the patient would be able to understand, avoiding technical terms.
The candidate should be able to ascertain the current level of
functioning and quality of life of the patient in a sensitive way, to
determine the appropriateness of dialysis (See Station 1 for a
description of types of dialysis).
Discuss the reasons for not coping with other renal replacement
therapy, e.g. CAPD.
Explore the patients expectations of CAPD and transplantation.
Explain that he has endstage renal failure and requires support. If
he is not managing CAPD, renal transplantation is the only
alternative, as haemodialysis has previously failed.
Explain the practicalities of obtaining a transplant: Cadaveric vs.
live donor, the waiting list is long, the length of wait for transplant
depends on finding an acceptable HLA match, explain the
complications of transplant, i.e. short-term (surgical risks), medium
term (immunosupression and risk of rejection) and long-term
(immunosuppression secondary malignancy and infection;
recurrent renal failure 5-year graft survival).
Ensure the patient understands what has been said. Ask if he has
any questions. Arrange a follow-up.
Lifestyle Adjustments
To illustrate two discussions of lifestyle, scenarios 17 and 18 tackle
the issues of smoking cessation and lifestyle adjustments following a
MI respectively.
245
SMOKING CESSATION
Scenario 16
Problem: Smoking cessation
Patient name: Ken Wood (aged 59)
Ken Wood is a 59-year-old bar manager who has been smoking 10
cigarettes a day for the last 20 years. His previous medical history is
otherwise unremarkable. His wife has mentioned to you that he would
like to give up smoking, and he has attended clinic today to discuss
this with you. You are the FY2/ST1 for General Medicine.
Explore his knowledge of the effects of smoking on health. Ask
about current smoking status. Explain that smoking cessation
reduces the risk of many diseases, including stroke, coronary artery
disease, peripheral vascular disease, COPD, cancers of the lung,
mouth, throat, larynx, oesophagus, pancreas, bladder, and peptic
ulcer disease (and in women ca of cervix and complications of
pregnancy).
Explain also the risk of smoking to others; that adults are at risk of
developing heart and lung disease from passive smoking.
Emphasise that there are social and cosmetic benefits from stopping
smoking.
Ask whether she has been given any quitting smoking leaflets.
Explain symptoms of nicotine withdrawal (such as tremor and
nausea). Inform about the benefits of stopping smoking. Involve
family and friends. Nicorette products and zyban (buproprion)
may help to avoid these withdrawal symptoms, but consider
contraindications include hepatic cirrhosis, seizure, CNS tumours,
EtOH withdrawal, benzodiazepine withdrawal.
Advise the patient to aim to stop completely rather than cut down.
Ask your patient if he/she really wants to stop smoking and if he/
she would be prepared to stop now or within the next few weeks.
Say that it may be useful to get rid of all ashtrays, lighters and
cigarette holders etc.
Find out whether previous attempts have been made, and what
measures helped/hindered.
Discuss ways of assisting, including setting a date and stopping
completely, enlisting the help of family and friends, enlisting the
help of health promotion services, and amfebutamone.
Watch out for relapse. Amfebutamone is a possible medication.
Advise the patient that he has access to specialist counsellors and/

or psychotherapists. Make appropriate follow-up arrangements.
Lifestyle adjustments after an uncomplicated acute myocardial
infarction
Scenario 17
Problem: Lifestyle adjustments after an uncomplicated acute MI
Patient name: Chris Goddard (aged 48)
Chris Goddard is a 48-year-old computer programmer who has just
sustained an uncomplicated anterior myocardial infarct. He was
successfully thrombolysed, with complete resolution of his ST changes.
You are the FY2/ST1 for Cardiology. He smokes about four cigarettes
a day, and drinks around ten pints of beer a week. He is about to be
discharged. He has been happily married for 15 years. He is keen to
discuss with you the lifestyle adjustments that will be necessary. Please
discuss with him, and advise accordingly.
Explore his knowledge of the term heart attack. Explain in simple
language what a heart attack is, i.e. it is caused by a blockage of a
blood vessel that supplies blood to the heart, but reassure him
that he has the correct and best treatment available and that he is
on the road back to health. Reassure him that many people do
well after a heart attack and that the reason for the tablets is to
offer some prevention from a second attack.
A patients specific concerns can be overlooked when giving advice
after a myocardial infarction (e.g. a flight to somewhere abroad in
a months time), because there are usually standard areas that are
usually discussed. Patients do not always voice their concerns.
Explain the need for tablets. Explain that he should change his
lifestyle, and tackle exercise, smoking and weight. Activity may
be restricted by an overprotective spouse. Returning to work
depends on the type of work and completeness of recovery. With
less physical jobs, 4-6 weeks off work is advisable. With physical
jobs, defer the return to work until after stress testing. Anxiety is
common. Most exercise programmes recommend at least three
types of aerobic exercise (e.g. brisk walking, jogging, swimming,
aerobics classes). Point out that regular exercise has benefits for
preventing further heart attacks and encourage him to go for walks.
Speak that you will speak to the cardiac rehabilitation nurse who
will arrange rehabilitation programmes. Offer pamphlets from the
rehabilitation team and the British Heart Foundation.
247
Say that he should not drive for a month and that he can have
sexual intercourse only after increasing his activity level, say to
going up briskly two flights of stairs. Explain the need for moderate
amounts of alcohol at maximum (e.g. around 21 units/week), as
heavy drinking can increase the patients weight and weaken the
heart muscle.
Ask if he has any questions. Offer appropriate follow-up.
INFORMED CONSENT
This section takes further some of the issues discussed in the previous
last section, namely, one aspect of medical practice is the approach a
doctor takes to obtain consent from a patient regarding investigation
and treatment for a given condition. Consent is only valid when the
individual is competent (or in legal terms has capacity). A patient is
not incompetent because they act against their best wishes. For consent
to treatment to be valid, the patient must be legally competent to
give consent, the patient must have sufficient information to make a
choice, consent must be given freely.
A competent patient can refuse any, even life-saving, treatment.
For example, in the case of Jehovahs witnesses, you may ask to explain
the benefits of blood transfusion, but you should allow the patient to
explain religious beliefs with respect. The use of components such as
albumin, immunoglobulins and haemophilia preparations may be
allowed on an individual basis. For normal blood transfusions, nonhaemolytic febrile transfusion reactions may occur, acute haemolytic
transfusion reactions, bacterial and viral contamination, wrong blood
group, iron overload, and circulatory overload (see Better Blood
Transfusion, 1998). Capacity is not a global term but is specific to
each decision, i.e. a patient may be competent to make a will but at
the same time incompetent to consent to treatment. A clinician does
not have to prove beyond all reasonable doubt that a patient has
capacity, only that the balance of probability favours capacity. The
critical stages in assessing capacity are: Comprehension and retention
of information needed to make a decision, ability to believe the
information, ability to weigh the information, consider the degree
and severity of risk to the patient, the risk to benefit ratio of the
treatment, the patients mental state, and ability make the decision.
Patients under 16 years of age can consent to treatment if they are
deemed Gillick competent, i.e. are deemed mature enough to
understand the implications of their actions.

A patient has a right therefore to refuse treatment ordinarily, but
not where there is an issue of public health. Section 37 of the Public
Health Act magistrates orders to allow compulsory treatment olf a
patient with notifiable disease. This is almost never needed if
appropriate negotiation with the patient is undertaken.
CONSENT AND THE LAW

This PACES station is not intended as a test of medicolegal issues,
but obviously candidates need to be roughly aware of them. The
main issues candidates are expected to know about are expressed
consent (consent either oral or in writing), statutory requirements
(where law requires particular consent for particular treatment), and
implied consent. At present, consent forms are used if a patient is
exposed to any invasive procedure. After providing the patient with
adequate information about the procedure, as well as risks and
benefits, doctors should document what has been said on the consent
form. The patient then reads the consent form with the doctor and
signs accordingly. The consent form provides a mechanism to ensure
that consent is obtained, and also to communicate the fact to other
members of the health team. Consent forms are not, themselves,
absolute proof that valid consent was obtained to the treatment
specified on the form. These tasks may be delegated to a person who
is suitably trained and qualified, with appropriate knowledge.
From a legal point of view, lack of consent engages two key aspects:
Battery/assault: Non-fatal offences against the person. A procedure
or treatment that is performed without consent.
Negligence: Harm caused by a doctor acting outside accepted
medical opinion or practice (the Bolam principle). If a patient does
not receive certain relevant information when consented for a
procedure, a doctor may be found negligent. It is advisable to tell
the patient of all potential serious complications and those with an
incidence of at least 1%.
Situations Where Consent is not Possible

A doctor, by acting in the patients best interests, can treat a patient
against their will under common law. The doctrine of necessity, which
underpins the treatment of patients lacking capacity, is made up of
the necessity to act and the action being in the best interests of the
patient, where a patient is unable to give the necessary consent
249
required for treatment. If relatives are available for discussion, they

should be informed rather than opinions canvassed. It is advisable
that they remain well informed. The patient has the right to be free
from discrimination, have privacy, have confidentiality of personal
health information with information disclosed only to the nominated
next of kin, liberty (i.e. free from interventions that inhibit liberty),
and continue dignity (according to social and cultural views). Legally,
when consent is not available and there is no advanced directive, the
responsibility for emergency operations rests with the consultant in
charge particularly if the team believes this is in the patients best
interests.
An advance directive is that a person can anticipate losing the
mental capacity to decide or communication how she wishes to be
treated by drawing up a formal advance statement of her values and
preferences or by naming a person who can be consulted. Whilst
advance directives may not always be legally binding or unambiguous,
it will be increasingly unwise to ignore these directives, and they can
be helpful to clinicians. If there is disagreement, a second opinion can
be arranged. Views about the patients preferences given by a third
party who may have more knowledge of the patient should be taken
into account. There are different types of advance directive.
If mental impairment is suspected, a psychiatrist may be consulted
to make the diagnosis. Medical staff may be required to make
decisions which are deemed to be in the best interests of the patient.
Be aware of the meaning of the following specific terms used in
relation to consent:
Proxy consent: A relative cannot consent on behalf of an
incompetent patient.
Implied consent: By going to hospital a patient should expect a
nurse to take their blood pressure and therefore consent for this
procedure should not necessarily be sought.
Emergency consent: Where consent cannot be obtained, medical
treatment can be provided to anyone who needs it.
Advanced directives or living wills: a patient makes a choice on
their future medical care before they become incompetent. A
doctor that treats a patient in the face of an advanced directive
could be liable in battery.
Power of attorney: A patient nominates a person (usually a relative)
whilst competent to make decisions on their behalf if they were to
become incompetent. However, this does not include medical

management decisions. With an increasingly elderly population,
there is growing need for people to delegate control of financial
and legal affairs to others close to them. A power of attorney is a
legal document enabling this to be done, allowing, for instance,
someone to sign cheques and letters on anothers behalf if he or
she were going abroad for some time; or if you became seriously
ill, or were mentally incapacitated, business and personal interests
could be looked after.
Ward of court: A doctor may apply to a judge to make medical
decisions on behalf of the patient. This is advisable if it is not clear
what the correct course of management should be and there is
opposition from colleagues or relatives against the intended
treatment.
MENTAL HEALTH ACT

The Mental Health Act [1983] (but please note Mental Health Act
[2007]) can be used to treat psychiatric illness in non-consenting
patients. This may be useful in patients who present with deliberate
self-harm either due to a temporary or permanent illness. Factors
suggesting suicidal intent include act in isolation, precautions to avoid
discovery, preparation made in anticipation of death, active
preparation for the event, leaving a suicide note; consider the events
preceding the act, concomitant psychiatric illness, personal and family
history, coping resources and the risk of suicide (male, < 19, > 45,
separate, living alone, chronic physical health, problems with alcohol
and drugs, psychiatric disorder including depression, schizophrenia
and alcoholism). They can be detained/restrained for varying periods,
depending on the clause of the Act, and can be given treatment, but
only for their mental illness, which is deemed in the best interests for
themselves or the public.
Section 5(2): Emergency Doctors Holding Power

Applied by one physician or an inpatient to enable a psychiatric
assessment to be made. 72 hours duration. Good practice to convert
this to a Section 2.
Section 2: Admission for Assessment Order

Applied by two written medical recommendations (usually a
psychiatrist and a GP) and an aproved social worker or relative, on a
251
patient in the community. 28 days duration. May be converted to a

Section 3. The patient has a right of appeal to a tribunal within 14
days of detention.
Section 3: Admission for Treatment Order

Applied as in a Section 2 on a patient already diagnosed with a mental
disorder. 3 months duration and then reviewed.
Section 4: Emergency Admission to Hospital Order

Applied by one doctor (usually a GP) and an approved social worker
or relative. Urgent necessity is demonstrable. May be converted to a
Section 2 or 3.
MENTAL CAPACITY ACT [2005]

This is an Act of the UK that came into force in April 2007. It applies
to everyone over the age of 16 in England and Wales. Its primary
purpose is to provide a legal framework for acting and making
decisions on behalf of individuals who lack the capacity to make
particular decisions for themselves The five principles are outlined in
the Section 1 of the Act. It aims to protect people who lack capacity to
make particular decisions, but also to maximise their ability to make
decisions, or to participate in decision-making, as far as they are able
to do so.
1. A person must be assumed to have capacity unless it is established
that they lack capacity.
2. A person is not to be treated as unable to make a decision unless
all practicable steps to help him to do so have been taken without
success.
3. A person is not to be treated as unable to make a decision merely
because he makes an unwise decision.
4. An act done, or decision made, under this Act for or on behalf of
a person who lacks capacity must be done, or made, in his best
interests.
5. Before the act is done, or the decision is made, regard must be
had to whether the purpose for which it is needed can be as
effectively achieved in a way that is less restrictive of the persons
rights and freedom of action.
Please note that this Act was amended by the Mental Health Act
[2007] in July 2007.
Examples of common consent scenarios:
ACQUIRING CONSENT FOR AUTOPSY

Scenario 18
Problem: Acquiring consent for autopsy
Relative name: Winnifred Thomas, wife of the patient Edward Thomas
(aged 84)
Edward Thomas, 84, was admitted yesterday with acute confusion.
He was tachypnoeic with a respiratory rate of 30/minute, and
cyanosed. His urea was 13 mmol/l, but his C-reactive protein was < 8
g/l. He was admitted to ITU, where an initial chest X-ray was
unremarkable. At 2 am this morning, he died suddenly. He had been
thought to have been suffering from a pneumonia, but this cause of
death was not certain. You are the ITU SHO. Your objective is to
inform his wife of his sudden death, and to acquire consent for an
autopsy if appropriate.
The principles of the breaking of bad news are outlined above.
Ensure that you will not be disturbed. In real life, you will also
ensure that you are appropriately dressed (e.g. not in blood-stained
theatre clothes).
Introduce yourself to the patient and establish rapport. Ask her if
she would like anyone else present at this point.
You must break the news about her fathers death early on. You
must provide the necessary background for the grave news, e.g.
the seriousness of the pneumonia, the expectation of her fathers
illness. Explain that attempts were made to contact her, but he
deteriorated suddenly and resuscitation was attempted. Avoid
making assumptions about the direct causes of any incident (e.g. a
drink-driver going off a road into the river) if there is a risk of
being judgmental. Mention that the death was swift and painless.
Avoid euphemisms for the death. Be prepared for the emotional
response, and be prepared to repeat information patiently.
Tell her how sorry you and all the staff who have looked after
him are.
Check if the relative has come alone or is with others if possible,
know who they are at least in general (the family).
If the relative would like to go on, explain that the doctors looking
after her father would like to know exactly what caused the sudden
deterioration. This can be done by performing a postmortem
examination. Ask if she knows if the patient himself had any known
objection towards a post mortem before his illness.
253
The relatives need a general understanding of the procedure. The

pathologist first carries out an external examination of the body,
before proceeding to an internal examination. Reassure her that
the body will not be disfigured.
Explain that she will be asked to sign a consent form.
Tell her that she can obtain the results of the post mortem as the
results are sent to thhe consultant looking after her father, and
she can arrange an appointment with him to have the findings
explained. Explain that the body can be viewed by relatives after
the post mortem if necessary.
Ask if she has any questions. Ask if she would like to contact
someone. Ascertain how much emotional support the subject has
in dealing with the bereavement.
If agreed, the medical certificate is issued before the post-mortem
so that the funeral arrangements can be made. Express condolence
and appreciate that the subject has maintained a major loss.
Allow the subject to speak and ask questions which should be
answered with sensitivity and empathy. Make follow-up
arrangements to speak to her or other members of the family again.
Offer to put them in touch with the transplant coordinator once
the family members have been consulted before reaching a decision.
Arrange immediate follow-up, e.g. further meetings with a Doctor,
including a GP.
Discussion
Organ and tissue retention at hospital postmortem examinations is
currently an issue attracting much public attention and is subject to
independent enquiries. Postmortems are introduced as a way of
discovering the cause of deterioration and are carried out by a
histopathologist according to standards set by the Royal College of
Pathologists, and may be full or limited in nature; if something
suspicious is found, consider objection to retaining of organ part for
educational or research purposes which can be kept indefinitely, or
disposed of in a legal and proper manner if the relatives change their
mind. Autopsies are useful where the cause of death is unclear, where
the disease is rare and an autopsy can shed new light on the disease,
and where information may shed light on other family members who
suffer from the condition. Coroners post mortems are required for
sudden unexplained death, deaths from an operation, suspicion of
unnatural cause of death (e.g. violence, neglect, drug poisoning). An
autopsy should not delay funeral arrangements, and relatives can

view the body afterwards. Finally, it is now widely accepted that
specific consent is required for organ/tissue retention. This issue is
an area of intense debate and leglislation is likely to be forthcoming.
The Human Tissue Act [1961] does not mention the requirement
for relatives of the deceased to consent to postmortem examination.
A donor card is sufficient legal authority to proceed; however, it is
good practice to assess the relatives wishes and few centres would
proceed if the relatives did not assent to organ donation.
Contraindications are infections such as HIV, prion disease, metastatic
tumours, severe atherosclerosis. Time delays involved prior to the
certification of death and the release of the body.
Regarding live organ donations, a donation may be obtained from
a non-genetically related person provided no payment is expected.
The Human Organ Transplants Act [1989] restricts transplants
between persons who are not genetically related. All proposals are
referred to Unrelated Live Transplant Regulatory Authority (ULTRA).
Living donor kidney transplantation is only considered if the risk to
the donor is low, the donor is fully informed, the consent is fully and
freely given, the donor can withdraw his consent anytime before the
operation, the offer of the organ is voluntary, and the transplant
procedure has a good chance of success. To sell an organ is illegal
(under s.16(1)). Please note that the UK currently does not operate a
system of presumed consent, where consent is assumed unless
notification is given otherwise. This is in contrast to some jurisdictions.
CONSENT FOR A HIV TEST

This is a relatively common examination scenario. We will therefore
attempt to consider the component parts of this discussion carefully.
Scenario 19
Problem: Acquiring consent for a HIV test
Patient name: Hannah Jones (aged 22)
Hannah Jones is a 22-year-old journalist who has a sore throat and
a rash. You have a clinical suspicion of HIV seroconversion. She has
recently returned from a trip abroad to SE Asia.
Discuss this possibility with her, and counsel her regarding an
HIV test.
A suggested plan for this consultation is:
Introduce yourself and try to establish a good rapport. The patient
must be aware that confidentiality will be respected.
255
Ask how the patient feels and explain that you are now in a position
to be able to tell her what the cause of the problem is.
A good candidate should consider a brief history of the current
illness as an introduction to the issue, and explore risk factors for
HIV infection so as to go onto sensitively introduce HIV infection
as a possible diagnosis. Ask her if she has been prone to infection
in the past.
The risk factors for HIV include current state of health, sexual
orientation, sexual behaviour (e.g. numbers of partners, type of
intercourse, use of condoms), partners, ethnic background (HIV-2
is common in parts of Africa), history of sexually transmitted
disease, sexual behaviour whilst overseas, history of drug abuse
(has she shared needles either now or previously), history of blood
or blood product transfusion here or overseas, or organ donation.
Review HIV risk reduction measures.
Discover the patients knowledge about HIV, how it is transmitted
and its prognosis. Avoid being judgemental. Review the natural
history of HIV infection.
Distinguish between anonymous and confidential testing,
availability of rapid-home-testing kits, and lab-send away from
home kit.
The candidate should be able to discuss the implications of a positive
test including who to tell and implications for employment. Include
that you can test for HIV infection, and not for AIDS. The window
period between infection and seroconversion is normally no more
than three months during which a false negative result may be
obtained. The course is usually transmission, primary HIV infection,
seroconversion, the asymptomatic period when lymphocyte counts
fall and then AIDS.
State explicitly that the test is for HIV antibodies, and it involves
talking a small amount of venous blood, tell the patient when the
result will be vailable, and tell the patient that the result will be
given verbally, ideally by you. The tests are ELISA and Western
Blot. Strict protection of client confidentiality must be maintained
for all persons offered and receiving HIV counselling services.
Explain that HIV is lifelong infection. Without treatment, there is
a relatively short life expectance due to immune suppression. New
drugs have revolutised the treatment with a marked improvement
in life expectancy. HAART treatment can now prolong life of
sufferers for up to 30 years. New treatments are being researched
all the time.

When applying for a mortgage, the patient may be asked whether
she have had an HIV test. If the test is positive, the patient will be
strongly encouraged to give consent for his GP and dentist to be
notified and the result will then be permanently be in his GP records.
The patient may be asked about his HIV status at employment
medicals, although they are not legally obliged to divulge
information. If positive, the patients partner(s) should be
informed. Say that you will not divulge details of the HIV test
(even if the test was negative) to any insurance company without
the patients consent.
You should assess the patients ability to cope with the implications
of a positive test and prepare them for it. Some implications of a
positive test are: It would need to be repeated to confirm its
positivity; it would give the patient greater uncertainty albeit of
an unpleasant nature; there might be social discrimination and
adverse psychological reaction; the patient would be offered
continued medical support including anti-retroviral therapy and
follow-up including prophylaxis of opportunistic infections
including appropriate vaccinations; it should motivate the patient
to practise risk minimization (decrease the number of partners,
condoms and spermicide, detoxification regarding i/v drugs, use
sterile needles, do not share razors or toothbrushes).
If the test is positive then all insurance policies taken out prior to
this will be honoured, although he may find difficulty in taking
out future policies; all prior policies will be honoured. There are
specialist companies for mortgages (and group-employment
schemes and opt-outs).
If the test is positive, it has to be considered that she may be at
risk of other transmitted viruses. For example, Hepatitis B and
hepatitis D which requires co-infection with Hepatitis B to replicate
successfully.
Ask who else needs to be told the result. Assess the personal and
social support, and advise the patient where to obtain information
about other services.
If negative, the possibility of a false negative has to be considered,
it might give the patient reassurance, and the patient will still have
to behave responsibility to minimise her risk of HIV. Explain about
seroconversion but dispel the false beliefs about immunity.
Having weighed up the pros and cons, the patient should be
encouraged to make a decision, and appropriate follow-up made.
257
(This question has featured in a number of different guises,

including oesophageal candidiasis, and hypoxia and abnormal CXR).
Discussion: Causes of a false negative ELISA (0.2%) Multiple
pregnancies, blood transfusions, liver disease, parenteral substance
abuse, haemodialysis, hepatitis B vaccination, rabies, influenza.
Causes of a false negative Western Blot (0.00001%)
Clerical error, contaminated sample, misinterpretation of results.
JEHOVAHS WITNESS
Scenario 20
Problem: Jehovahs witness requiring blood transfusion
Patient name: Kirsty Fox (aged 42)
Kirsty Fox is a 53-year-old church volunteer. She presented with a
history of tiredness, palpitations, raised blood pressure 180/110
mmHg. CT of the abdomen revealed that she has a large
phaeochromocytoma on the right side adjacent to the aorta. She is
about to undergo an operative procedure to remove the
phaeochromocytoma. She has a past medical history of having three
TIAs within the last year. However, in view of the position of the
tumour, there is a high risk that the patient may bleed, making blood
transfusion a critical matter.
Jehovahs witnesses refuse to take any blood or blood products,
they refuse any blood to be reintroduced to their body. They
regard this as a sin.
This patient needs the operation. There is a high risk that the patient
will bleed. And if the patient continues to refuse the surgeons
may have the right to cancel the procedure, if he/she feels the risk
is more than the benefit. So you are left with a dilemma, if he/she
feels the risk is more than the benefit. So you are left with a
dilemma that you need to convince the patient of the necessity for
the blood.
It is difficult if you know little about their beliefs. Tell me a little
more about your faith. Your best option is first to build a rapport
and find out how much the patient knows about the condition.
Their confidentiality is paramount; it is up to them, if they take
blood and does not inform the church. Explain the options: EPO
but the patient is hypertensive. Another possibility is re-introducing
ones own blood (amount-limited and the period to save it in the
fridge is also limited). Offer her the option of discussing this with
the elders of the Church.

Bring to her attention the watchtower policy. When it comes to
fractions of any of the primary components, each Christian, after careful
and prayerful meditation, must conscientiously decide for himself. Refer
to the Bloodless Surgery Centre (the Watch Tower Society has
lists).
Be aware of patients refusal or childrens consent best interests
principle/only one parents consent required.
ETHICAL ISSUES REGARDING GENETIC COUNSELLING

Consent is clearly crucial in situations regarding genetic counselling.
This type of task poses particular problems.
The principles of genetic counselling whatever the condition
The subject should be encouraged to select a companion for the
stages of the testing process: The pretest stage, the taking of the test,
the delivery of the results and the post-test stage. The tests performed
are:
Carrier-testing: Usually for AR/XLR conditions to base reproductive
decisions. Give information regarding reliability of test, implications
of carrier status. Children are advised to delay this until old enough
to make personal decision.
Predictive testing: Presymptomatic tests: Usually for complete
penetrance AD conditions, e.g. HD. If no useful treatment, the value
of testing is questionable. This has profound implications regarding
insurance, etc.
Predisposition testing: Increased risk, not certain of disease (e.g. BRCA
for breast cancer, APO for Alzheimers disease).
The aim of genetic screening is to identify people who might benefit
from the new medications, help genetic researchers understand the
disease better and so lead to improved treatment, and help people
plan for the future. However, the disadvantages are that a genetic
defect cannot be repaired. Neither prevention or cure is possible. The
test may not accurately predict who will develop the disease; testing
positive does not necessarily mean that a person will definitely develop
the disease and testing negative does not guarantee they will not.
There could also be an effect of a positive test on buying property,
getting insurance and financial planning for the future. Alternatives
the applicant can consider are not to take the test for the time being,
to deposit DNA for research, and to deposit DNA for possible future
use by family and self. Discuss how the diagnosis relates to others,
259
e.g. mother: social aspects, legal aspects. Counsellors and

multidisciplinary team (such as a geneticist, neurologist, social worker,
psychiatrist, or medical ethicist) are important. Consider socioeconomic
consequences on potential employment, social security, data security
etc. Reassure the patient that there will be time to decide if he is
unsure about proceeding and that at the next appointment you will
provide information about addresses of support services. Say that
you could refer him to a regional genetic centre if he wishes to go
ahead with the testing.
Discussion
The subject must choose freely to be tested and must not be coerced
by anyone. Extreme care should be exercised when testing would
provide information about another person who has not requested
the test. This issue arises when an offspring with a 25% risk requests
testing with full knowledge that his or her parent does not want to
know his or her own status. Ownership of the test result remains
with the subject who requested the test.
HUNTINGTONS DISEASE AND GENETIC COUNSELLING:

EXPLAINING A TEST RESULT
Scenario 21
Problem: Explaining a test result (genetic test for Huntingtons disease).
Patient name: Anne Wood (aged 37).
Anne Wood, aged 37, has attended clinic following the recent diagnosis
of her mother with Huntingtons disease five years ago, which
followed a 2 years history of psychiatric disturbance and choreiform
movements. She agreed to have a genetic test for Huntingtons disease.
You are the FY2/ST1 for Neurology. She has returned to clinic to
discuss with you the results of the test.
Introduce yourself to the patient and establish rapport. Ask if she
would like someone with her.
Establish the patients beliefs about the disease (Huntingtons
disease), her concerns and expectations. She must be aware of the
seriousness of the condition and its untreatable nature. If she is
not fully aware, the doctor should discuss the nature of the disease
at length with her, including its inherited nature. Before moving
on, ask if she has any questions about the disease.
Explore why she has decided to have the test now. Explain that
the test is positive.

At this point wait for the patients reaction.
If the patient is not emotionally well prepared, listen and answer
questions. The patient may not wish to talk about siblings or
children at this point although she may already be aware of the
inherited nature of the disease.
If the patient is well prepared, ask if she has thought about telling
other members of her family, the implications of inheritance and
who may or may not be affected.
Discuss support groups. Ensure that the patient has adequate
emotional support at home.
Summarise the discussion. Ask if she has any questions. Arrange
follow-up.
DIFFERING PATIENT RESPONSES

In real life, we have to acknowledge that people, in response to certain
situations, all tend to react differently. This is reflected in the
description of the station provided by the Royal Colleges of Physicians
in Station 4. Candidates are expected to react to these different patient
responses appropriately. In real terms, in the exam, do not allow the
actors to wind you up you need to show that you can keep calm
even when stressed. Consider the following examples:
1. If the patient is angry, acknowledge the anger and plight. Listen
without interruption. Avoid being defensive. Check how intense
the anger is. Keep calm and do not raise voice. Empathize. Advise
of complaints procedure. Offer to meet later.
2. If the patient is depressed, ask her to tell you more about feeling
low and the extent of it (severity, frequency, comparison with
how the patient feels normally). Direct questions may be aimed at
particular symptoms, for example, sleep, concentration, loss of
interest, loss of energy, loss of appetite, loss of weight.
3. If the patient is confused, check their orientation according to time,
place and date, and assess their short-term memory by giving them
a name and address to remember and check their recall
immediately. Assess whether they are having any abnormal
experiences (e.g. misinterpretations, hallucinations), and whether
there is any evidence for false beliefs such as delusions. Give the
patient a clear explanation of their confusional state, and to reassure
them that this is why they are having a confusional state. It is
important to explain that every effort will be made to determine
the cause of the confusion.
261
4. If communicating cross-culturally, ask him if there is anything

special about his culture (e.g. sense of family) or religion that might
be affecting him. Show acceptance of this cultural or religious
dimension, and explore the patients views. Avoid the danger of
stereotypying in cross-cultural communication, by accepting that
each person has their own particular view of culture or religion.
Express solutions and involve other agencies if possible.
5. If communicating through an interpreter, address both the patient
and the interpreter, and communicate simply in chunks. Be aware
of some problems involved with using interpreters (e.g. incorrect
transmission or misunderstanding of information, avoidance of
delicate topics, domination of the patient by the interpreter).
6. When talking to someone who is over-talkative, avoid interrupting
too much because the more you interrupt the more your patient
will tend to have to say; steer the patient by selectively reflecting,
paraphrasing and summarising aspects of the narrative, avoid
resorting to closed questions until you have developed some sort
of rapport, and, most of all, remain calm and courteous.
A MEDICAL MISTAKE AND AN ANGRY PATIENT

Scenario 22
Problem: Medical mistake (omission of a gentamicin level)
Patient name: George Ellis (aged 48)
George Ellis is a 46-year-old man who was commenced on
ciprofloxacin and gentamicin on this admission for an acute
exacerbation of bronchiectasis, but who has previously been admitted
on multiple occasions with infective exacerbations of bronchiectasis.
His previous medical history included multiple respiratory infections
as a child. The drug chart indicated that he was supposed to have a
gentamicin level on the 3rd dose, but this was accidentally omitted.
He has found out about the error. This is the first time such a mistake
has happened. He had been told yesterday that his renal function
was normal. You are the FY2/ST1 for Respiratory Medicine. He would
like to discuss the problem with you.
Introduce yourself to the patient and establish rapport. Explain
involvement in the case.
Tell the patient that there has been a problem with one of the
drugs. Explain the concept of a therapeutic range and the need to
monitor levels.
Explain what happened and how.

Apologise for the error. Emphasise openness and truthfulness.
Allow the patient to voice anger. Empathise and give legitimacy
to the patients feelings. Show your empathy verbally and nonverbally.
Say that you are disappointed.
Explain the side-effects of the drug (e.g. problems with
deteriorating kidney function), and that therefore appropriate
monitoring will be necessary (for example, blood tests).
Explain the steps that you have taken to determine the cause and
to prevent it from happening again. Explain the need for continuing
medical care.
Deal with emotions before facts; put the emotions into words and
offer them back to the patient. Seek to understand the emotions.
Be clear what the patient is feeling and identify the source of these
feelings.
Encourage the patient to elaborate on the background of his
emotions. Avoid disagreement.
Explain the possibility of further action for him to take in the future,
e.g. formal complaint, and identify constructive actions that you
and the patient can take.
State that you will discuss the mistake openly with your consultant,
an adverse incident form will be completed, and that the
conversation will be documented in the medical notes.
Ask the patient for any further worries.
The conditions for negligence are that the doctor owes a duty of
care, that the doctor was in breach of the appropriate standard of care
imposed by the law, and that the breach in the duty of care caused
harm in question.
Bolam v Friern Hospital Management Committee [1957] is the English
case that lays down the typical rule for assessing the appropriate
standard of reasonable care in negligence cases involving doctors.
The Bolam test provides that where the defendant has represented
him or herself as having more than average skills and abilities, this
test expects standards which must be consistent with a reasonable
body of medical opinion (De Frietas v OBrien [1995] which suggests
that this can be as low as 11 in 1,000 doctors). It is intuitive, and the
common law position, that this standard of care must not be palpably
wrong (Bolitho v City and Hackney Health Authority [1997]), although
the law does allow for different, nut valid, possible management
decisions.
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CONFIDENTIALITY AND GOOD CLINICAL PRACTICE

Under common law, doctors are obliged to maintain confidentiality,
and MRCP(UK) candidates are expected to respect that confidentiality
forms the core of any doctor/patient relationship. In terms of ethical
principles, confidentiality therefore supports the principle of respect
for patient autonomy, a principle that emphasises the patients right
to have control over his own life. The fundamental concept of medical
confidentiality is that patients have a right to expect that information
about them will be held in confidence by their doctors. Without
assurances about confidentiality, patients may be reluctant to give
doctors the information that they need to provide good care. The
doctor must also respect requests by patients that information should
not be disclosed to third parties, except in specific circumstances, where
the health or safety of others would otherwise be at serious risk. The
issue of when it is lawful, and when it is not lawful, for a doctor to
breach confidentiality is often a question of balancing public interests,
and of balancing private and public interests. The General Medical
Council provides professional guidelines on the issue of confidentiality
for practising doctors. Whilst these do not have the force of the law,
they are taken seriously by the courts.
OBLIGATIONS FOR DOCTORS TO BREACH MEDICAL

CONFIDENTIALITY
The GMC(UK) states that patients have a right to expect that doctors
will not disclose any personal information which they learn during
the course of their professional duties unless they give permission.
Indeed, several acts of Parliament allow access of patients to material
kept about them (the Data Protection Act, the Freedom to Health
Records Act (1990) and the Freedom of Information Act (2005)). When
a doctor is responsible for confidential information, it is the duty of
the doctor to ensure that the information is effectively protected against
improper disclosure when it is received, transmitted, stored or
disposed. When patients give consent to disclosure of information
about themselves, you must ensure that they understand what is being
disclosed, the reasons for disclosure, and the likely consequences.
You must also ensure that patients are informed whenever information
about them is likely to be disclosed to others involved in their health
care (sharing information with other members of the healthcare team
is not generally viewed by the law as breaching confidentiality), and
that they have the opportunity to withhold permission. Confidential

information must be disclosed in the following situations. If
confidential information is disclosed, the doctor should release only
as much information as is necessary for that purpose.
When legally required by a court order
In a communicable disease notification, and the reporting of births,
deaths, abortions and work-related accidents (Public Health
Control of Diseases Act 1984; Abortion Act 1967; Births and Deaths
Registration Act 1953). This is a statutory duty.
Identification of patient undergoing in vitro fertility treatment with
donated gametes (The Human Fertilisation and Embryology Act,
1990).
Identification of donors and recipients for transplanted organs
Human Organ Transplants Act 1989.
Drug addiction (Misuse of Drugs Act, 1973).
In cases of national security, such as terrorism or major crime
prevention or solution (Prevention of Terrorism Act, 1989).
Police on request name and address (but not clinical details) of
driver of vehicle who is alleged to be guilty of an offence under
the Road Traffic Act, 1988.
Confidential information may be disclosed at a doctors discretion:
When a 3rd party is risk of harm, for example, at risk of contracting
a serious infectious disease,
When it is in the public interest, e.g. patient with seizures known
to be driving illegally,
Through sharing information with the health care team
Other than for treatment only with express consent (e.g. lawyers,
Insurance companies).
In terms of public interest, the doctor is advised to disclose
information promptly to an appropriate person or authority. Examples
of this include a situation where a medical colleague who is also a
patient is placing the patient at risk as a result of illness or another
medical condition.
No information that might identify a patient examined or treated
for any sexually transmitted disease should be provided to a third
party, except for in a few specific situations where that third party
may be in a situation of contracting a life-threatening disease, such as
HIV infection. Furthermore, doctors should not write reports or
disclose any confidential information which may be requested by
insurance companies or employers without the patients prior written
consent.
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Even after a patient has died, the obligation to keep the information
confidential remains. If an insurance company seeks information about
a deceased patient to decide whether or not to make a payment under
a life insurance policy, information should not be released without
the prior consent of the patients executor, or a close relative, without
being fully informed of the consequences of disclosure.
Possible consequences of breach of confidentiality are loss of trust,
disciplinary action by the GMC, civil legal action, and investigation
of serious professional misconduct by the General Medical Council.
Disclosure of information and public versus private information.
A Road Taffic Offence

In road traffic offences, the doctor must breach confidentiality and
provide the police constable with the name and address of the patient
(Road Traffic Act [1988]). The doctor must explain that he cannot without
the patients consent divulge any other information which can be used
to prevent minor crime, or help convinction in minor crime. Most
crimes against properties are onsidered to be minor crimes now.
Details should not include clinical details. You are duty bound by a
duty of confidentiality not to give any clinical information without
the consent of the patient. Most crimes against properties are
considered to be minor crimes now. Similarly, the doctor cannot breach
confidentiality to prevent minor harm to another individual.
Fitness to Drive
The DVLA is legally responsible for deciding if a person is medically
unfit to drive. They need to know when holders of a driving licence
have a condition which may now in the future affect their safety as a
driver. The following situations illustrate the steps taken in discussing
this with patients. The ethical areas in the fitness to drive scenarios
are respecting confidentiality, recognising the need to inform others
when a patient refuses to take responsibility, recognising that failing
to act may put others at risk, and recognising that a doctors duty
may involve doing something to which the patient has not consented.
EPILEPSY
Scenario 23
Problem: Epilepsy and DVLA
Patient name: Terri Warner (aged 21)

Terri Warner is a 21-year-old night club dancer who was admitted
yesterday with a second tonic-clonic seizure. She had a similar seizure
a month previously. Both seizures occurred whilst at work, in the
presence of strobe lighting. She had been working the night shift,
and had felt relatively tired on both occasions. She has undergone a
MRI which is normal, and an EEG demonstrated abnormal activity in
relation to light stimuli. Her only medication is the oral contraceptive
pill. She normally drives to work. Please discuss with her the results
of her investigations. She is keen to carry on driving, especially off
road driving, a competitive sport which is not governed by the DVLA.
Introduce yourself, explain your role clearly, and agree the purpose
of the interview.
Explain epilepsy in a way that a layperson would understand. A
seizure is a sudden, unpredictable attack of electrical activity of
the brain resulting in shaking of part of the body (or all four limbs).
It may cause you to lose consciousness. Epilepsy is a term we use
when somebody is having seizures.
Establish the patients level of knowledge of precipitating factors,
including alcohol and recreational drugs, lifestyle and late nights.
Inform her that alcohol will lower the fit threshold, and the
medication given to avoid further fits may not work properly.
Avoid swimming, bathing alone, cooking alone with gas cookers,
heights. Ask about understanding of medication: Important issues
are compliance and pill-failure, and continue anti-epileptic
medication with folate cover during pregnancy.
Ask about her occupation. Remember that with every epilepsy
scenario, it is very important that you ask what the persons
occupation is since their medical condition may prevent them from
safely carrying out their job.
Ask about driving and state how this would affect the persons
life and job. Make sure that the patient understands that the
condition may impair his ability to drive.
Provide information about the law in relation to epilepsy. A patient
can drive (on and off drugs) when they have been free of fits for
12 months, provided that they do not have continued high
likelihood of seizures (e.g. a known brain tumour). If he/she has
purely nocturnal (sleep) seizures he can drive, provided this pattern
has been established for 3 years. Advise the patient about his
responsibilities to himself and other drivers.
The onus is on her to report the condition to the DVLA. The patient
must be aware that you have the right to inform the DVLA if you
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think that the patient is going to continue to drive despite careful

consideration of the position. Mention lack of insurance cover if
they drive and safety issues. Remain calm in the face of mild
aggressive and emotional behaviour by the patient.
If the patient refuses to accept the diagnosis or the effect of the
condition on driving, you can suggest that the driver seeks a second
opinion. You should advise that the patient should not drive until
the second opinion has been obtained.
Notice that she is a young woman of childbearing age. You need
to tell her that certain anti-epileptics can make the oral contraceptive
pill less effective and that a doubling or even tripling of the dose
of oestrogen may be required. It is important to also inform her
that pregnancy can ina percentage of women result in fetal
teratogenic side effects. Explain that the risk is around 7%
compared to 3% for the normal population and that there are
ways of minimizing the risk, e.g. taking folic acid, using one instead
of two anti-epileptics and possibly using the newer agents.
Inform about the British Epilepsy Society. Agree a plan by the end
of the interview. Advise her about the need to inform her partner.
Arrange for appropriate follow-up.
The framework for the interview is likely to include: respect of
the patients autonomy (i.e. the capacity of the patient to make
deliberated or reasoned decisions for himself and to act on the basis
of these decisions), disclosure of confidential information (i.e. it is in
the best interest of the public if this information is handed to the
relevant authorities).
Table 7.1: Summary table of the DVLA and common medical disorders. For further
information, please see consult www.dvla.org.uk for current guidelines.
Disease
Private vehicle license
HGV
Epilepsy
MI
1 year fit free

1 month
Stroke
IDDM
1 month
Notify DVLA
Fit free, off medication

3 months. Symptom-free. Completes
9 minutes Bruce-treadmill test
Banned
Banned
Public Health
A patient may refuse treatment ordinarily, but Section 37 of the Public
Health Act, 1984, magistrates orders to allow compulsory treatment
of a patient with notifiable disease. This is almost never needed if
appropriate negotiation with the patient is undertaken, which is a
good thing as it is very difficult to work.
Compulsory Treatment of TB
The Public Health Act (Control of disease) [1984] states that, in exceptional
circumstances where a person with TB of the respiratory tract poses
serious risk of infection to others, a CDC and Respiratory Physician
can enform compulsory admission of the patient.
Needlestick Injury
If you or another health care worker has suffered a needlestick injury
or other occupational exposure to blood or body fluids and you
consider it necessary to test the patient for a serious communicable
disease, the patients consent should be obtained before the test is
undertaken. If the patient is unconscious when the injury occurs
consent should be sought once the patient has regained full
consciousness. If appropriate, the injured person can take prophylactic
treatment until consent has been obtained and the test result is known.
If the patient refuses testing, is unable to give or withhold consent
because of mental illness or disability, or does not regain full
consciousness within 48 hours, you should reconsider the severity of
risk to yourself, or another injured health care worker, or to others.
You should not arrange testing against the patients wishes or without
consent other than in exceptional circumstances, for example where
you have good reason to think that the patient may have a condition
such as HIV for which prophylactic treatment is available. In such
cases you may test an existing blood sample, taken for other purposes,
but you should consult an experienced colleague first. It is possible
that a decision to test an existing blood without consent could be
challenged in the courts, or be the subject of a complaint to your
employer or the GMC. You must therefore be prepared to justify
your decision. If you decide to test without consent, you must inform
the patient of your decision at the earliest opportunity. In such cases
confidentiality is paramount: Only the patient and those who have
been exposed to infection may be told about the test and its result. In
these exceptional circumstances neither the fact that test has been
undertaken, nor its result, should be entered in the patients personal
medical record without the patients consent. If the patient dies you
may test for a serious communicable disease if you have good reason
to think that the patient may have been infected, and a health care
worker has been exposed to the patients blood or other body fluid.
You should usually seek the agreement of a relative before testing. If
the test shows the patient was a carrier of the virus, you should follow
269
the guidance in paragraphs 21 - 23 of this booklet on giving information

to patients close contacts.
END OF LIFE DECISIONS

This chapter concludes with the area in medical ethics that raises
probably the most strong and diverse views: Those concerned with
end-of-life decisions. Indeed, topics such as euthanasia, do not
resuscitate orders, and even advance directives (living wills) concern
many outside the medical profession.
Who Makes End of Life Decisions?

Doctors, patients and families may face the question of how actively
life-sustaining treatments should be pursued. In making these
decisions, there should be respect for the patient autonomy, knowledge
about the limitation of the treatment and promotion of the patients
best interests. Patients are deemed to act autonomously if they act
with intent, with understanding and without controlling influences.
Patients of this calibre may refuse life-prolonging treatment. If the
patient knew all the relevant facts, there is reason to limit lifeprolonging treatment. If the desires are regarding treatment, then it
needs to be clear whether the decision was formed with an adequate
understanding of alternatives and their consequences, and that these
decisions were made when the patient was competent, and formed
without coercion. If this is the case, there is no reason to limit lifeprolonging treatment. In some situations, the opposite scenario may
arise when a patient requests life-prolonging treatment which may
prove harmful or futile. If the patient has made this decision, having
been fully advised, there is no reason to satisfy the request.
Doctrine of Double Effect

The principle of double effect permits an act which is foreseen to
have both good and bad effects. This doctrine distinguishes actions
that are intended to harm versus those where harm is foreseen but
not intended. Frequently, doctors set out to relieve pain and suffering
but see that life may be shortened. Foreseeing is not necessarily the
same as intending. This is in keeping with duties of a doctor. Consider,
for example, patients dying from cancer. These patients are often given
heightened dosages of opiates to relieve pain by their medical care
teams who willhave foreseen that these actions may shorten the
patients life by their effects on respiratory depression. Although it

would be morally wrong to inject morphine into the patients blood
stream with the intent of hastening death, it may not be necessarily
wrong to inject it if the foreseeable consequences of it were to hasten
death if the doctors intention was to relieve pain.
Euthanasia and Assisted Suicide

Euthanasia is intentional killing, i.e. murder under English law, and
therefore illegal. Assisted suicide, i.e. helping someone take their own
life, is a criminal offence.
Arguments for: Respecting a patients autonomy over their body,
beneficence (i.e. mercy killing may prevent suffering), suicide is legal
but unavailable to the disabled.
Arguments against: Good palliative care obviates the need
euthanasia, risk of manipulation / coercion/ exploitation of
vulnerable, undesirable practices when constraints on killing
loosened.
Physician-assisted suicide is where the physician provides
patient with the means to commit suicide.
Euthanasia and assisted-suicide are illegal.
for
the
are
the
Best Interests
Options for treatment or investigations are contemplated by the
Medical Team which are clinically indicated are in line with the
patients expressed preferences, and the patients background
(cultural, religious or employment), or the patients preferences given
by a 3rd partner.
Advance Directives
Advance directives are not covered by legislation. In cases of conflict
with other legal provisions, advance statements are superseded by
existing stature. A person can anticipate losing the mental capacity to
decide or communicate how much he or she wishes to be treated by
drawing up a formal advance statement of her values and preferences
or by naming a person who can be consulted. These are statements
usually written and formally witnessed made by a person when they
are fully competent about the medical care he/she does or does not
want to receive should they become incompetent in the future. It will
be increasingly unwise to ignore these directives, and they can be
helpful to clinicians. Advanced consent is not legally binding, e.g. to
271
be kept alive as reasonably possible using whatever forms of treatment

are available. Advanced refusal is legally binding if adult and
competent when made, the decision was informed, circumstances have
arisen which were envisaged, and the patient was not unduly
influenced.
Withholding Medical Treatment

The primary goal of medicine is to benefit the patients health with
minimal harm, and this should be explained to those close to them so
that they can understand why treatment is given, and why a decision
to withhold or withdraw life-prolonging treatment may be considered.
Balance should be in favour of treatment if there is doubt. On the
other hand, treatment may prolong suffering and there is no absolute
ethical or legal right to a treatment that may prolong suffering. When
a patient lacks capacity to make decisions and there is uncertainty
about the appropriateness of treatment, treatment that may be of
some benefit should be started until clearer assessment can be made.
This is particularly important in emergencies, when more time is
needed for detailed assessment. Although, it may be emotionally easier
to withhold treatment, rather than to withdraw that which has already
been started, there are no legal or necessarily moral distinctions
between the two. The BMA considers that where a particular treatment
is no longer benefitting the patient, continuing to provide it would
not be in the patients best interests and maybe morally wrong. Greater
emphasis on the reasons for providing treatment including artificial
nutrition and hydration, rather than the justification for withholding
treatment, may challenge this perceived difference (British Medical
Association, Withholding and withdrawing life-prolonging medical
treatment: guidance for decision-making, 1999).
Whilst the nature of the withdrawal of medical treatment will
depend on the particular context, we hope that the possible structure
to this difficult area below is a useful guide:
In withholding treatment, you may start by suggesting you wish
to share some thoughts on the next step if the outlook is poor.
Explain that the team feels that continuing active treatment will
not achieve the desired result and introduce the concept of
withdrawing active treatment. This does not mean the same as
withdrawal of all treatment. Explain that, rather, the emphasis
will change from treatment with the aim of cure or prolongation
of life to that of the relief of symptoms and for the promotion of

the patients comfort and dignity. The quality of care will remain
the same.
In explaining this situation, it can be helpful to go back over the
past history and place the severity in historical context. Ask if any
members of the family have had views on this, or whether the
patient had views on this when well.
Explain that the patient is not in pain and well sedated. Explain
that if the family allows the withdrawal of treatment, he may
deteriorate quickly and die soon after.
Point out politely that the final decision of withdrawal of treatment
does not reside with the family but the ITU staff. Explain how the
withdrawal will be undertaken.
Explain that a decision is not needed right away, and ask about
any queries.
The case of Burke v GMC [2005] suggests that artificial nutrition
and hydration (ANH) cannot be withdrawn without a court order, in
other words ANH rights may reside with the patient. ANH should
not be withdrawn where there is doubt/disagreement about the
patients capacity, where a lack of consensus amongst doctors
regarding prognosis or best interests, where the patient when
competent may have wanted ANH to continue, where the patient
resists/disputes the withdrawal of ANH, and where close others feel
that ANH withdrawal is not in the patients best interests.
Do-not-attempt Resuscitate (DNAR) Order

English law does not require doctors to prescribe futile treatments,
even if requested so by the patient. Therefore a DNR order is an
example of limiting treatment that is futile. Cardiopulmonary arrest
is the most crucial of all medical emergencies. Local Trusts have their
own regional guidelines usually authored by a Resuscitation Committee
and ratified by the Executive Board.
The BMA, RCN and UK Resuscitation Council (1999) state that a
DNAR order is appropriate:
a. Where CPR is unlikely to be successful.
b. CPR is not in accord with the recorded sustained wishes of the
patient if mentally competent.
c. CPR is not in accord with a valid advanced directive.
d. CPR is likely to be followed by the length and quality of life not in
the best interest of the patient. Expected benefits are outweighed
by the burdens, e.g. life-burdened by severe uncontrollable pain,
permanent lack of awareness, or total dependency.
273
Possible definitions of futility include: the likelihood of the patient

regaining consciousness following resuscitation is less than 1%, the
likelihood of the patient being in hospital following resuscitation is
less than 10%, or the patient will love only for a few weeks because of
another untreatable terminal illness. The resuscitation decision is made
by appropriate health professionals and not by the patients relative,
but her cooperation is valued; address all concerns of the relative.
This decision should be made after appropriate consultation and
consideration of all aspects of the patients conditioning. Emphasise
the need for self esteem, dignity and comfort. Ask if other members
of the family need to be involved, and consider their spiritual beliefs.
Doctors should make a decision as to whether to inform the patient
of the decision. It may be inhumane and distressing to raise issues of
this nature with terminally ill patients. However, ideally the patient
should be fully informed of any discussions about care and decisions
regarding resuscitation. The order should be conveyed to all members
of the multi-disciplinary team, and reviewed in light of changes in
the patients condition. A DNAR order can sometimes be made without
consulting a patient if there is no likelihood that resuscitation would
be successful (futility), or if the patient is not able to make such a
decision (unconscious or not competent to do so), or if the patients
quality of life is extremely poor.
DNAR
Scenario 24
Problem: Do-not-attempt-resuscitate order (DNAR)
Patient name: Tony Graham (aged 62)
Tony Graham, aged 62, was admitted with a stroke. Following
management of this stroke, a palliative stent was inserted for his
underlying disease, carcinoma of the head of the pancreas, but it is
known that he has a very poor prognosis given that he now has
metastases in the liver. He was discussed in your multidisciplinary
team meeting this morning, and the Consultant signed a form to state
that, in the event of a cardiopulmonary arrest, a resuscitation attempt
should not be made. He has never discussed this issue with your
team. You are the FY2/ST1 for General Medicine. Your Consultant
would like you to discuss this resuscitation status with him.
Setting: A quiet office to ensure a lack of interruptions.
Pacing: Allow yourself enough time.

Opening: Introduce yourself and establish good rapport. Call yourself
Doctor. Ask how to address the patient.
Give a warning shot. I have something important to discuss with you.
Establish the patients understanding of the underlying condition
and reason for admission. Emphasise that he on maximum medical
therapy which will continue, including strong antibiotics for the
chest infection and medications to relieve any distressing or
suffering.
Ask an open question about how his symptoms have been recently.
Good listening skills prepare for the most difficult part of the
interview.
What does he think will happen on the future?
Explain there will be a decline in his function, i.e. a grave prognosis,
and the reasons for this. Somebody with a condition as bad as yours
may suddenly take a turn for the worst.
Respond to emotions. I see that you are distressed by the situation. I
find it very hard to confront you with painful facts like this.
If we were to restart your heart, we might prolong a situation which you
find intolerable. We would hate to do the wrong thing for you. If your
heart were to stop beating, would you want us to restart it for you?
If he feels strongly that he would like every medical attempt made
to prolong his life, this should be respected.
Ask what he/she feels about this. Promise support from doctors
and nurses. Agree treatments to relieve symptoms.
If he does not wish to be resuscitated, you could say something
like, I can see how distressing it is for you to face up to how ill you are.
I can see that its a hard decision for you, but you said that life is so bad
that you wouldnt want your heart to be restarted. Have I understood you
correctly?
If he does not wish to be resuscited, you could explain to him that
death is not a failure, and that the decision has been taken to let
nature to take its course.
Explain that the patient should be left comfortable with the aim of
preserving dignity and self-esteem.
Explain that a side-room will be organised for privacy. Ask if there
are any other members of the family who need to be involved.
Finally, address any other concerns of the patient.
Say when you will meet again.
In most circumstances, a patient should be involved in a DNAR
decision. It should be borne in mind that for every patient there comes
a time when death is inevitable and cardiac or respiratory function
275
will fail. It is essential therefore to determine for each patient whether

CPR is appropriate. A DNAR order should only be given after full
consultation with the patient and the medical team. Where a patient
is seriously ill, decisions about CPR should be ideally made in advance.
The current guidelines are that if the patient is not competent to take
part in the decision, consider discussing the issue with family to help
make the judgement. If the length and quality of life after resuscitation
is likely to be worthwhile, do not consider a DNAR order; else DNAR.
The DNAR order should be reviewed and documented at a frequency
appropriate to the patients condition. The most senior available
member of the medical team is normally responsible for entering the
DNAR decision, and the reasons for it.
Medicolegal Aspects of Care of the Elderly

Although the law applies to everyone, there are certain aspects which
become particularly associated with the needs of elderly persons.
Testamentary Capacity
The law requires that a person making a will has a sound disposing
mind. Doctors are often asked to assess a patient prior to making a
Will. It is important that accurate records are taken and kept of the
assessment in order that your decisions can be justified by
contemporaneous note keeping.
In addition to establishing and documenting the absence of
cognitive impairment it is necessary to specifically assess the following:
Does the patient understand the nature of the act of making a Will
and its effects?
Does the patient know the nature and extent of his/her property?
Does the patient know which persons have a claim upon his/her
property?
Can he/she form a judgement on the strength of the claims made
by these people on his/her property?
Has the patient expressed him/herself clearly and without
ambiguity (this need not necessarily be in writing as nods and gestures
can be allowed)?
Section 47
Section 47 National Assistance Act [1948] gave the Medical Officer of
Health the power to apply to a Magistrate for the compulsory removal
of persons who:are suffering from grave chronic disease or being

aged, infirm or physically incapacitated, are living in insanitary
conditions AND are unable to devote to themselves and are not
receiving from other persons proper care and attention.
The Section 47 Act is not commonly used with only around 250
cases admitted per annum in the whole of the UK. It is good practice
that Geriatricians be involved and it is probably better that patients
compulsory detained are initially admitted to hospital where they
can be given the full benefit of a medical assessment.
Power of Attorney
This is a legal document which gives total control of a persons financial
affairs to someone else. It must be made by a mentally competent
person but ceases to be valid once the patient loses the mental capacity
to withdraw it. This is only really of any use for physically incapacitated
patients who wish their attorney to deal with their affairs.
Enduring Power of Attorney

This is a document taken out by a person when they have mental
capacity, which will continue if it is subsequently lost. This is the
preferred method for elderly persons to safeguard their financial
affairs and property. It does not relate to decisions regarding medical
treatment.
Once it is decided that mental capacity is lost the Enduring Power
of Attorney must be registered with the Court of Protection. This
usually requires that the document is accompanied by a doctors
opinion that the patient has now lost the mental capacity to make
decisions. The patient concerned is notified and if they disagree and
feel that they have not yet lost their mental capacity they may challenge
the decision so providing some safeguard. It is wise that two attorneys
are established, one person being a family member (usually a grownup child) and the other to be the representative from a legal firm.
Court of Protection
This is an Office of the Supreme Court of Judicature under the
direction of a master, deputy master and assistant masters. The Courts
primary function is to safeguard the financial interests of a patient by
providing for his/her maintenance and that of his/her family
dependants and management of his/her propert, and the Public Trustee
is a specific person to whom these powers are delegated. It can take
months to grant receivership which is usually granted to either a firm
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of solicitors or to a relative, but the Court itself has to oversee all the
expenditure which it must also approve. This is really the only
mechanism of controlling the financial affairs of a mentally incompetent
patient if no Enduring Power of Attorney has been produced. This is
extremely expensive and is not to be recommended if it can be avoided.
The family solicitor will usually arrange for the patient to be
examined by a doctor who will determine whether or not the patient
is capable or incapable of managing and administering his/her property
and affairs by virtue of mental disorder. The patient is usually served
with notice of proposed proceedings so they may protest if they feel
they have not yet lost their powers. The doctor may choose to
recommend that the service of notice is dispenses with if either the
patient is incapable of understanding it or that service would be
injurious to health or for any other reason.
The Court of Protection is usually receptive to providing things
which will improve the quality of life of a patient. For example, they
may well fund a holiday for both themselves and their carer and may
be in a position to approve purchase of a vehicle, if funds permit, in
order to allow for trips out, etc.
CONCLUSION
We hope that the scenarios above help to illustrate some of the key
principles underlying the communication skills and ethics which are
being tested. The key mistake to avoid is to think you must have a
script ready for every discussion before you attend the examination.
All consultations are different, and relying on a pre-prepared formula
may be dangerous if you are seen to not respond to the patients
needs. Practice with somebody this station in advance of the
examination, and consider whether the principles you apply for the
examination are being appropriately applied in real life. It is intended
that people who pass this station in the examination are performing
well in their day-to-day careers.
REFERENCES
Communication skills for Doctors. Peter Maguire. Arnold (Hodder
Headline Group) (2000).
Ethics and Communication Skills. Medicine 2000; Vol 28:10.
Royal College of Physicians. Clinical guidelines for candidates: the
PACES examination (2001).
PRACTICE QUESTIONS
1. Mr. Giles, a 55-year-old man, is due to be reviewed in clinic as a
follow-up patient. He has been diagnosed as having type II
respiratory failure, in the presence of chronic obstructive
pulmonary disease. Pulmonary function tests have shown:
FEV1 is 0.95 pre b-agonist (predicted value 3.5 l)
FEV1 is 1.29 post b-agonist.
He has gross ankle oedema. At present, he is on salbutamol and
atrovent mdi inhalers. Please discuss future potential
management strategies and Mr Giles understanding of his disease
process with him.
2. Mr. Johnson is a 46-year-old man who has undergone
investigations for a six-month history of pain and stiffness in his
joints, predominantly affecting the small joints of his hands, wrists
and ankles. The blood tests have revealed the following:
Normal FBC, normal biochemical profile other than mildly
elevated liver function tests and significantly elevated ESR and
CRP.
The rheumatoid factor is positive at 1 in 320.
X-ray of the hands have revealed early erosions.
He does enjoy regular pints of beer with his friends at his local
pub. He has returned for his follow-up appointment. Please inform
him of the diagnosis and the potential of management strategies.
You would ideally like to start him on methotrexate.
3. Miss Salt is a 19-year-old lady who was diagnosed as an insulindependent diabetic six years ago. She is due to be discharged
following a five-day in-patient stay after her third recent episode
of diabetic ketoacidosis. You are seeing her prior to her discharge.
Please advise her regarding her diabetic control.
4. The son/daughter of a 74-year-old woman with severe
rheumatoid arthritis has demanded to see a doctor now and
you have complied with this request. The patient was admitted
four weeks ago with a UTI but has become weaker and less
mobile. She has bed-sores and today swabs have revealed MRSA.
5. Please respond to the referral letter below.
Re: Jane Francis
(aged 32)
Dear Doctor,
I would be very grateful if you could see Mrs. Francis urgently.
She has attended with a itchy skin rash on her elbows, and I
wonder whether she could be started on suitable treatment for
6.
7.
8.
9.
10.
279
this. She lives with her two children aged 6 and 4, who have also
developed some itchy lesions. She has been trying to maintain a
diet compatible with her diagnosis of coeliac disease. She seems
anxious.
Yours sincerely,
You are a registrar. This patient has been diagnosed with acute
renal failure, the creatinine is climbing despite appropriate
treatment, and he/she is likely to need to commence
haemodialysis tomorrow. He/she has a past history of
nephrectomy for renal cell cancer treated at another hospital;
you know few details about this, but the patient looks well and
has been leading a relatively normal life until he/she became
acutely ill three days prior to admission. However, his wife
reports that he has also had diabetes for 10 years, treated with
oral hypoglycaemic agents. The patient is in a high-care ward on
a cardiac monitor with central line. You have come to explain
about the need for dialysis.
You have just been phoned by the Nuclear Medicine department
to say that a V/Q scan on a 35-year-old woman gives a high
probability of pulmonary embolism. Your task is to explain the
prognosis, and the need for treatment with warfarin. You should
give the patient appropriate information to take this drug safely.
Mr. Peters has had open tuberculosis. He has a young family
who have all received a course of chemoprophylaxis. He, to date,
has fully-sensitive mycobacteria on sputum culture. He admits
to being non-compliant with therapy. This is the second time
that he has had to recommence treatment. Discuss the importance
of completion of treatment with Mr. Peters and how this can be
achieved.
John Harvey is a 65-year-old lorry driver who was discharged
last week following a myocardial infarction. He has been found
to be in atrial fibrillation (a new finding since his MI), but does
not appear symptomatic with him. Please advise him about his
concerns.
A 35-year-old cyclist is referred to you, with recurrent syncope
of unknown cause. He loses consciousness without warning for
30s. He is advised not to cycle in public roads, but refuses to
agree to this as he cycles as a city courier-delivery service for his
job. Counsel him regarding his cycling. What legal restraints are
available to prevent him from cycling?

11. You are the medical FY2/ST1 on call. You are asked to come
urgently to the A&E department where Mrs. Brown has
presented with 24 hours of haemoptysis and a two-month history
of cough, purulent sputum and weight loss. Urgent staining of
the sputum has revealed plentiful Mycobacteria (Ziehl-Nielsen
staining). The A&E FY2/ST1 says that previous notes of the patient
had been found and that a diagnosis of rifampicin and isoniazid
resistant tuberculosis and been made 18 months previously. The
patient had taken treatment for three months in an isolation unit
in hospital before going home. She had been lost to follow-up
and discontinued treatment after discharge. The patient is not
keen to be admitted as she did not enjoy isolation and would
prefer to be at home, looking after her disabled husband. Your
task is to discuss with the patient:
The need for further investigation (including contributory
underlying factors)
The need for treatment
The need for admission
What can be done for the household contacts?
12. Mr. Brown is a 61-year-old man who was fit and healthy until
one year ago now has end-stage cardiac failure. He is not a
candidate for heart transplantation because due to his age and
degree of renal failure. He was admitted routinely by yourself
to optimise his cardiac failure therapy but his condition has
deteriorated over the weekend as your team forgot to decrease
the dose of his diuretics. His renal failure worsened. The ITU
team have reviewed him and refused an HDU or ITU bed due to
his terminal condition. The family has requested a meeting with
you, and the senior nurse looking after the patient feels a decision
on resuscitation should be raised.
13. A 59-year-old man, Mr. Patel, has severe congestive cardiac
failure. He has idiopathic dilated cardiomyopathy. The strict
upper age group for heart transplantation is 60 years. He recently
turned 62, and has developed insulin-dependent diabetes mellitus.
He has been on the waiting list for three years. His cardiac
function has deteriorated. He is keen to discuss the possibility of
heart transplantation.
14. The son/daughter of a patient with a slowly progressive primary
brain tumour has asked to discuss discharge plans. The patient
has been in hospital for three weeks, can only transfer with the
help of two people, and is intermittently confused. 24-hour
15.
16.
17.
18.
19.
20.
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nursing assessment suggests that discharge home would only be

possible with an acre package comprising two carers three times
a day. Carers are in short supply and this is not feasible. Nursinghome placement is the only option.
A normally fit 74-year-old has suffered a dense right-sided stroke
and is unconscious. You have arranged to see a spouse to discuss
decision-making about intravenous hydration and whether or
not to institute enteral nutrition.
An endoscopy is carried out on Mr. Hopkins, a 37-year-old
gentleman who has presented with weight loss and epigastric
discomfort. Endoscopy has revealed severe oesophageal
candidiasis. The risk of immunosuppression had not been
considered when he was initially reviewed. You are to review
Mr. Hopkins during his follow-up clinical appointment. Please
inform him of the findings of the gastroscopy and discuss the
further potential management plans with the patient.
You are the FY2/ST1 in the Genitourinary clinic. Mr. Jones is a
Consultant Surgeon in your local hospital. His wife is diagnosed
as HIV positive. She does not wish her husband to be told. She
is, however, concerned about the risks of his job to other people.
She wants to know if Mr. Jones should be asked not to operate
on patients this afternoon. Please counsel her.
A 30 year old man has presented with CMV colitis. He has
returned to clinic for the results of a HIV test that is positive. He
is married and his wife is expecting her first child. Explain the
news to the man, discuss telling his wife, discuss the possible
risks to the child, and introduce the idea of a multidisciplinary
team approach.
This in-patient who is in his/her 40s presented with a short
history of jaundice. ERCP has diagnosed a carcinoma of the head
of the pancreas. You have come to him/her to explain the
diagnosis and possible treatment options.
Mr. Evans is a 42-year-old man who has admitted following an
episode of haematemesis and melaena. He was treated with
variceal sclerosis during endoscopy and required four units of
blood transfusion during acute admission. He is now no longer
encephalopathic and has been haemodynamically stable for the
past 48 hours. This gentlemans liver disease has been diagnosed
to be purely related to his heavy alcohol consumption. Please
advise him as you feel appropriate.

21. You have just gastroscoped this patient with symptomatic acid
reflux and found a hiatus hernia with oesophagitis. You now
have got to see the patient to explain the results of the gastroscopy
and outline the treatment options medication, surgery.
22. Mr. Jones is a 25-year-old pharmaceutical representative. He has
been referred to you by his general practitioner. Mr. Jones was
involved in a road-traffic accident whilst on holiday in Spain. He
suffered head injuries from which he made a full recovery.
However, 6 hours post trauma, and on the way to the local
hospital, he had a grand mal seizure. This was treated by the
paramedics with lorazepam. He was discharged from the hospital
on carbamazepine. He has not returned back to work yet, though
it has been 3 months since the incident. He feels cognitively
impaired and low in mood. He has asked to see you because he
has been told he cannot drive for 3 years, and is unsure how he
can regain his life back.
23. Complaints about your house officer have been made by the
nursing staff. Sometimes rude, short-tempered, he/she is causing
moderate friction on the ward. You need to try and sort things
out.
24. You are the medical FY2/ST1 on-call and asked by the A&E staff
to attend a patient who has presented with a hypoglycaemic
attack. He has had some intravenous dextrose, and is now awake
and orientated. This is the first hypoglycaemic episode which
required hospital treatment. Your task is to convince Mr. Watkins
of the need to revoke his driving licence and persuade him to
inform the DVLA.
25. You are seeing the daughter of a 87-year-old lady who is ill
following an extensive CVA. You wish to discuss her
management, particularly nutrition, but the family seem unkeen
on any further treatment. The patient has written a will with an
advance directive asking to be resuscitated if required.
26. You are the SHO on the ward. You have been asked to see the
son of a patient of yours, Mr. Irvine. He lives a long distance
from his father and sees him only 2-3 times per year. Mr. Irvine
is an elderly man with metastatic carcinoma of the lung. He is
admitted with an acute episode of breathlessness and a large
pleural effusion which has confirmed malignant cytology. He is
very cachectic and very frail. He lives alone since his wife died 4
years ago. He claims that he has had enough and feels too unwell
to undergo any further treatment. You feel that he is competent
283
to make this decision. Your task is to discuss Mr. Irvines

prognosis and decide with his son:
The idea of further investigation
Any proposed treatment
The likely prognosis and resuscitation status.
27. You are the medical FY2/ST1 doing a ward round. You have
been told by the Nurses that the wife of one of your patients
would like to speak to you before you review her husband. He
has severe Chronic Obstructive Pulmonary Disease and has been
admitted with an infective exacerbation. He is on home nebulisers,
home oxygen and is housebound due to a combination of his
lung disease and depression. On the ward, he is receiving
intravenous antibiotics and an aminophylline infusion as well as
his regular nebulisers and oxygen. Mrs Smith does not want her
husband to be resuscitated in the event of a cardiac arrest. Mrs
Smith is depressed, tired and fed up with her husbands illness.
She feels that whilst she would like to continue to care for him,
she also cannot watch him suffer any more. She would like to
discuss his resuscitation status with you, but does not want him
to know, as it would upset him. She feels that he should not be
resuscitated but would like this decision to be made without her
husband. Your task is to explain that whilst resuscitation is likely
to be futile, Mr Smith must be involved in all decisions regarding
his care and that will include discussions about his resuscitation.
Focussed Clinical
Problem (Station 5)
[The authors recommend that, particularly for this chapter, you consult
a good quality atlas of clinical medical images.]
In the old examination, there were about five minutes allocated
for each of the minors. These correspond to short cases of the old
MRCP format. The second half of this chapter includes descriptions
of the skin, endocrine, locomotor, and eyes cases which can now appear
in any of the four preceding stations. However, as of May 2009, the
Station 5 has now changed such that it now contains a focussed clinical
problem. This is because the part of the old examination was seen as
artificial, and the new format of the assessment is a better reflection
of what a Registrar in higher specialist training, or a Consultant, would
have to do in real life given the time limits of genuine clinical practice.
PART 1: THE NEW FORMAT OF THE EXAMINATION

You will be assessed on your ability to demonstrate each of the seven
clinical skills described below. Each Station tests a fixed combination
of these skills. The main categories of the assessment include: Physical
examination, identifying the physical signs, clinical communication,
differential diagnosis, clinical judgment, managing patients concerns,
and maintaining patients welfare (Please see the MRCP website: http:/
/www.mrcpuk.org/PACES/Pages/PACESChanges.aspx).
There will now be two 10-minute encounters at this Station rather
than the current structure in which candidates see four patients for 5
minutes each.
The encounters will each take the form of a Brief Clinical
Consultation in which the patient presents with a single clinical
problem or symptom of the sort encountered in day-to-day practice
in the wards, receiving unit or outpatient clinic. You will be required
to undertake a brief focussed history and brief targeted examination
Focussed Clinical Problem (Station 5)
285
in the 8 minutes available with the patient, before discussing findings

and diagnosis with the examiner for 2 minutes.
It is not necessary for you to undertake a full, comprehensive
history (as required in Station 2) or a thorough, systematic examination
(as required in Stations 1 and 3) in these encounters but to demonstrate
a focussed and integrated clinical problem solving approach.
All the scenarios will be structured to ensure that a capable
candidate can undertake the task within the time available. Real or
simulated patients may appear in these encounters. The four disciplines
currently represented at Station 5 will not always be represented in
the examination, but clinical problems relating to those disciplines
(dermatology, ophthalmology, endocrinology, and rheumatology; see
PART 2 of this chapter) will frequently appear at Stations 2, 4 or 5, so
candidates must continue to be prepared to assess patients whose
problems primarily relate to these systems. Patients with problems
relating to disciplines or areas less clearly represented in the current
examination, for example, acute medicine and elderly medicine, may
now also be encountered. The structure of all other Stations, and the
overall duration and timings of the examination remain unchanged.
The pass mark will be defined by a formal standard setting process
that will also take close account of the current PACES pass standard.
It is intended that the overall standard of the examination will remain
the same; that is, the examination overall will be no harder or easier
to pass.
Development of This Station

There were a number of significant problems with the old MRCP
PACES Station 5. The clinical cases are presented most commonly as
spot diagnoses and do not assess the candidate on the competencies
described in the curriculum for General (Internal) Medicine (Acute),
which is the aim of PACES. The old Station 5 had been shown, in
fact, to contribute the least to the discrimination between candidates
performance in the examination overall.
In real life, the key competencies of a doctor are the ability to take
the history and interpret it, the ability to examine a patient and
appreciate the clinical signs, and the ability to communicate with a
patient appropriately and respond to concerns raised. These skills
are tested separately at Stations 1 to 4 in PACES but they are not
assessed in an integrated fashion as used every day in clinical practice.
The new Station 5 has been subject to rigorous pilots with
feedback from current examiners. From the candidates point of view,

time management in this Station is vital, in demonstrating a competent
response to what is a potentially complicated series of problems within
a patient. The methods of history taking and communication described
in full in the other chapters will enable one to acquire these skills.
Also, the approach to identifying and analyzing physical signs will
enable one to be proficient in this Station. A correct examination should
be focussed to allow to formulate a detailed lists of likely conditions
that may occur, and the lists of differential diagnosis in the preceding
chapters will help.
Marking Scheme
Most of all, the candidate will need to demonstrate a pragmatic
approach in the following areas:
a. Diagnosis, investigations and management will help one be
proficient at clinical judgment;
In practice, the doctor would be expected to make
recommendations for further investigations to determine the initial
diagnosis and subsequent managent, and act on the results for the
benefit of the patient. Here, it is worth stressing that the function
of the consultation is to address the problems of the patient, not
any underlying diagnosis.
b. Addressing patients anxieties and concerns will enable one to be
proficient at managing patients concerns.
This could involve responding to mood clues, exploring the
patients health beliefs.
c. Clinical skills, investigation and management (an action plan)
will enable one to address and maintain patient welfare.
The welfare of patients is at center of medical care, either at the
level of delivering technical welfare (e.g. prescribing painkillers to
an elderly lady with rheumatoid disease) or delivering social welfare
(e.g. arranging for volunteers to attend an elderly lady who is housebound with rheumatoid disease). Such social interventions may include
pastoral support and providing practical and financial advice to
improve quality of life. The critical aspect to note with regard to this
(and similarly for Station 5) is to know when exactly to call for specialist
assistance, and how to do so. The balance between the provision of
these types of welfare varies enormously between specialties, between
personalities and consulting styles, and between views of the role of
doctors.
287
The case is supported by papers similar to those used at Stations 2

and 4. Thus, the candidate is introduced to the case by a very short
note:
This: 76-year-old attended this morning for day surgery on her cataracts.
and she mentioned that she had noticed swelling of joints in her hands. Your
task is to assess the problem by means of a relevant history and a focussed
physical examination.You should then advise the patient of your probable
diagnosis, and your plan for investigation or treatment as appropriate.
The patient has a short narrative giving agreed history detailing
her complaints and the information she would like from the candidates
consultation with her. The examiner will observe the history-taking,
the examination, and the communication with the patient. The examiner
would not be able to assess whether the candidate had accurately
identified any physical signs that may be present, and might also
have difficulty appreciating the differential diagnosis in the candidates
mind from observation of the encounter. For this reason, the only
interaction between candidate and examiner is when the candidate is
requested by the examiner to report the clinical findings and give the
differential diagnosis.
The new Station 5 is supposed to mirror everyday clinical practice
the Brief Clinical Consultation whereby a junior physician is asked
to see a patient in the ward or in the clinic who raises a particular
problem.
PART 2: REVISION NOTES ON SKIN, LOCOMOTOR,

ENDOCRINE AND EYES
Please note that the history of any of these disorders could be assessed
as part of the History Taking Station (Station 2), and the examination
of any of these disorders could be a part of any of the Clinical stations
(Stations 1 and 2).
SKIN
Please look at the skin here (a certain part of the body) and discuss
your findings.
Description
All pigmented lesions should be defined by size (Increasing or not),
site, shape, presence of satellite lesions, bleeding, pruritus,
pigmentation, associated lymphadenopathy, and features of systemic
upset (history of drugs/medications, allergies, contacts with similar
rash).

A few important definitions.
Macules: A flat, circumscribed area of discoloration; if >1 cm this is
termed a patch.
Papules: A circumscribed elevation of the skin < 1 cm in diameter.
Plaques: A raised flat-topped lesion > 1 cm.
Bullae: A fluid-filled lesion (blister) > 1 cm.
Vesicles: A circumscribed fluid-filled elevation less than 5 mm in
diameter.
Pustule: A pus-filled lesion.
Wheal: A raised compressible area of dermal oedema.
Scale: Flakes arising from abnormal stratum corneum.
Crust: Dried serum, pus or blood.
Telengectasia: Permanently dilated, visible small vessels.
NEUROFIBROMATOSIS
Multiple neurofibromata, caf-au-lait spots (normal person may have
up to five), axillary freckling, Lisch nodules (melanocytic harmartomas
of the iris). Neurofibroma are soft or firm mobile subcutaneous lumps
or nodule around peripheral nerves.
Extra points: Hypertension (associated with renal artery stenosis
and phaeochromocytoma), fine crackles (honeycomb lumb and
fibrosis), neuropathy with enlarged palpable nerves.
Inheritance is Autosomal Dominant

Two non-allelic inheritable forms. Type I is classical peripheral form
(associated with chromosome 17; there may be an association with
other tumours of the CNS such as optic glioma, meningioma,
glioblastoma, and, rarely, phaeochromocytoma; also iris harmartomas),
type II is central and presents with juvenile cataracts, bilateral acoustic
neuromas, meningiomas and gliomas and sensori-neural deafness
rather than skin lesions (autosomal dominant, associated with
chromosome 22).
Associations: Pheochromocytoma (2%) and renal artery stenosis (2%).
289
Complications: Epilepsy, sarcomatous change (5%), scoliosis (5%),

mental retardation (10%). Spinal nerve root formation can lead to
cord compression. CNS fibromas can lead to stenosis/compression of
the Sylvian aqueduct and give rise to hydrocephalus.
Investigations: Genetic screening, 24-hour urinary catecholamines,
MAG-3 scan for renal artery stenosis, MRI brain/spine (type I), MRI
cerebellopontine angle, auditory testing (type II).
Management: Condition is autosomal dominant and therefore genetic
counselling; surgery where appropriate.
Complications: Acoustic neuroma, Vth nerve neuroma, cord
compression, sensory loss and Charcots joints, lung cysts, intracranial
tumours, associated with phaeochromocytoma (need to check BP),
nodules on iris and hamartoma of the retina.
ECZEMA
Eczema is an inflammatory skin disorder with characteristic histology
and clinical features, that include itching, redness, scaling and a
papulovesicular rash. Eczema can be divided into two broad groups:
Exogenous and endogenous.
Erythematous, lichenified patches of skin.
Predominantly flexural.
Scaling.
Fissures (painful), especially hands and feet.
Excoriations (a shallow abrasion due to scratching).
Secondary bacterial infection.
Differential diagnosis: Exogenous (primary irritant dermatitis and
allergic contact dermatitis) and endogenous (atopic a characteristic
dermatitic eruption associated with a personal or family history of
atopy, the age of onset being between 2 and 6 months, with males
more affected than females, tends to be chronic but tends to improve
during childhood; discoid (nummular) well-demarcated patches on
the trunk and limbs; pompholyx itchy vesicles on palms and soles,
seborrhoeic dermatitis red, scaly rash caused by Pityrosporum ovale,
occurring on the scalp, face and upper trunk and more common in
young adults and HIV patients, gravitational, asteatotic).
History and examination are sufficient for diagnosis. Investigations:
History of atopy, e.g. asthma, hayfever and allergy; patch-testing
(useful in establishing potential allergic contact) and prick testing.
Complications: Secondary infection and erythroderma.

Treatment: Avoid irritants, exacerbating factors and precipitants;
regular emollients, tar bandages, wet wraps, antibiotic ointment for
minor infections; topical steroids; anti-histamines for pruritus;
antibiotics for secondary infection; u/v (UVB or PUVA) light therapy.
Also consider topic tacrolimus, pimecrolimus (recent NICE review
available).
VITILIGO
Key signs are depigmented lesions.
Investigations: None although Woods light will highlight but not
fluoresce like a fungal lesion. Consider other autoimmune problems
such as thyroid/pernicious anaemia.
Management: Usually cosmetic, camouflageRed Cross run a service.
Phototherapy, topical steroid and tacrolimus have been tried with
some benefit but seldom really good results.
Sun protection.
PSORIASIS
A genetically determined, inflammatory and proliferative disorder
of the skin, occurring in 1-2% of the UK population.
Aetiology unknown. Association with HLA Cw6, B13 and B17 in
skin disease and B27 in psoriatic arthropathy.
More common in 2nd and 6th decades, with females generally
developing psoriasis at a younger age than males.
Numerous symmetrical well-demarcated/sharply-defined salmon
pink/red plaques of varying sizes with silvery white scaling surfaces.
The plaques are most prominent on extensor surfaces (elbows, knees)/
scalp and hairline/behind the ears/at the umbilicus. Extent of severity
of plaque psoriasis, presence of variant psoriasis, presence of
arthropathy.
Koebners phenomenon: Localised at the site of trauma (other causes
include lichen planus, vitiligo, viral warts, molluscum contagiosum).
Auspitzs sign: Punctuate bleeding spots on scraping the scales. (Other
associations are lichen planus, viral warts, vitiligo and sarcoid). Note
the character of the lesions (scales, thickness, erythema, pustulation),
the extent of cover, the degree of itching, and complications such as
joint involvement. Skin staining from treatment.
Types: Pustular-palmoplantar pustukosis variant, yellow/brown sterile
pustules and erythema affects palms and soles.
291
Erythodermic psoriasis: Severe systemic upset with fever, raised WBC,

inflammatory markers and dehydration; confluent areas affecting most
of the skin surface.
Flexural psoriasis: Affects axillae, submammary areas and natal cleft.
Often smooth, red and glazed looking.
Guttate: An acute eruption of multiple drop-like lesions on trunk
and limbs following a streptococcal infection.
Palmo-plantar pustular psoriasis.
Nail psoriasis: Include keratin thickening; loss of minute plugs of normal
keratin results in characteristic pitting and sometimes the thickened,
dystrophic nail separates from its nail bed; subungual hyperkeratosis,
destruction of the nail plate, discolouration of the nail plates and
oncholysis. Other causes of oncholysis (often with discoloured,
thickened, hyperkeratotic but brittle dystrophic nails) include fungal
infection, trauma, dermatitis, peripheral vascular disease,
thyrotoxicosis.
Chronic plaque: Well-defined disc like plaques covered by white scale
classically affecting elbows, knees and scalp.
Associations with psoriasis: Gout, arthropathy, malabsorption (Crohns
and ulcerative colitis).
Factors which exacerbate psoriasis: Trauma (Kobner phenomenon),
infection (including HIV), endocrine (psoriasis generally tends to
improve during pregnancy and deteriorate during the post-partum
period), drugs (-blockers, lithium, antimalarials and the withdrawal
of oral steroids can exacerbate psoriasis), alcohol, stress (severe
physical or psychological stress).
Investigations: Most patients do not require any investigations. Skin
biopsy can be used to detect psoriafirom papillomatosis, acanthosis,
hyperkeratosis and parakeratosis, with intradermal collections of
neutrophils.
Treatment: A careful explanation of the disease process and the likely
necessity for long-term treatment should always be given. The type
of psoriasis and severity influences the choice of treatment. It is usual
to use topical agents as the first-line treatment.
Topical (emollients such as oil/soap emollients and moisturisers
control scale), calcipotriol ointment (vitamin D3 analogues), coal tar
(smell, stains brown), dithranol (stains purple and burns normal skin,
usually effective), topical retinoids such as tazarotene, hydrocortisone.

For widespread or severe disease, further treatment options
include:
Systemic: Cytotoxics (methotrexate and ciclosporin: Methotreate is used
in widespread plaque, acute generalized pustular and erythrodermic
psoriasis, and psoriatic arthropathy as short-term or maintenance
treatment; retinoids are effective particularly in acral or generalized
pustular psoriasis), retinoids (acitretin, safe and teratogenic)
Phototherapy: UVB narrowband (311-313 nm) is now replacing
broadband UVB (290320 nm) (for chronic plaque and guttate
psoriasis), psoralen + UVA (PUVA).
Other biological agents (promising new treatments but as yet not
licensed for psoriasis include etanercept and eflalizumab, presently
under review by NICE): Efalizumab humanized monoclonal antibody
blocks T cell activation/migration; alefacept recombinant fusion
protein which interferes with activation/proliferation of T cells;
etanercept human fusion protein of the TNF receptor which acts as
a TNF? inhibitor; infliximab monoclonal antibody which binds TNFa.
Complications: Psoriatic arthropathy 10% (five forms: DIP involvement,
large joint mono/oligoarthritis, seronegative, sacroilitis, arthritis
mutilans), erythroderma.
Guttate psoriasis: Associated with streptococcal throat infection, resolves
in 3 months.
PURPURA
These fall largely into two groups.
Vessel disorders.
Platelet disorders.
Observe the distribution of the lesions, e.g. senile purpura/steroids
often affect backs of hands and forearms. Henoch-Schonlein purpura
classically appears over lower limbs and buttocks. Scurvy over lower
limbs/backs of thighs with perifollicular haemorrhages plus corkscrew
hairs; look for woollen gums.
Inspect palate for petechial haemorrhages, gums for ulceration and
haemorrhage (suggests neutropenia and thrombocytopaenia),
conjunctivae and fundi for haemorrhages (fundal haemorrhages only
in severe thrombocytopaenia).
Look for evidence of cause: Cushingoid (steroid), Rheumatoid,
SLE, infective endocarditis, Chronic liver disease, Ehler-Danlos
syndrome.
293
If a vasculitic cause is suspected, it is important to look for renal

involvement; you should therefore offer to dipstix the urine.
DERMATITIS HERPETIFORMIS
Look for characteristic distribution on extensor surface of elbows,
knees and on occiput, interscapular and gluteal regions. These are
symmetrical, highly itchy vesicles or urticarial plaques on the trunk
and extensor surfaces, buttocks and occasionally the face and scalp,
and is associated with gluten-sensitive enteropathy (coeliac disease).
Dapsone is the treatment of choice.
KAPOSIS SARCOMA
There may be solitary or numerous reddy-purple, and bluish-brown
macules, plaques and nodules. These may occur on the skin and
mucosa.
Sites commonly affected: Skin, feet, mouth, stomach, lungs.
Lesions can be painful.
Systemic disease may cause abdominal pain or haemoptysis.
Endemic in African males, peripheral involvement.
In HIV +ve patients, distribution may be widespread.
Lymphatic obstruction leading to chronic oedema and cellulitis of
lower limbs.
Also seen in elderly Jewish or Meditteraneam males, with indolent
course on distal extremities, and in immunodeficient patients,
including transplant patients.
Investigations: Biopsy and PCR for HHV-8, CD4 and viral load,
endoscopy and bronchoscopy if symptomatic.
Treatment: Radiotherapy often useful for patients with oedema,
interferon alpha, chemotherapy.
BUTTERFLY RASH
There is a butterfly malar rash. Look for/consider causes:
1. Systemic lupus erythematosus: There are raised or flat patches of
malar erythema, sparing nasolabial folds. Other areas such as the
forehead and neck and often unaffected. There may be marked
photosensitivity. There may be mouth ulcers, Oral ulceration,
Scarring alopecia, Anaemia. Vasculitic changes in the hands.
Raynauds phenomenon. Jaccouds arthropathy (mimics rheumatoid
arthritis but due to tendon contractures not joint destruction).

Typical arthropathy involves MCP and PIP joints, ulnar deviation
of the joints, sublaxation of the PIP joints. Elsewhere: Purpura due
to thrombocytopenia, livedo reticularis, pyoderma gangrenosum,
peripheral oedema. Extra points: Respiratory (pleural effusion,
pleural rub, fibrosing alveolitis), neurological (focal neurology,
chorea, ataxia), eyes (Sjogrens), renovascular (hypertension,
proteinuria).
Diagnostic investigation: ANA, anti-dsDNA.
Disease activity: Elevated ESR but normal CRP, elevated
immunoglobulins, reduced complement, urine microscopy
(glomerulonephritis). FBC, APTT, anti-cardiolipin antibodies if
APTT prolonged.
Treatment:
Mild
disease
(topical
corticosteroids,
hydroxychloroquine), moderate disease (prednisolone,
azathioprine),
severe
disease
(methylprednisolone,
cyclophosphamide, azathioprine). Specific photoprotection advice
includes using skin creams or makeup, and avoidance of sun at the
middle of the day.
2. Discoid lupus erythematosus: DLE is a skin limited disease with well
defined erythematous papules or plaques on light exposed areas
including the head, neck, hands and arms. The lesions are scaling
and hyperkeratosis of hair follicles gives these scales a dotted
nutmeg appearance. If you were to remove the scales and inspect
their undersurface, you would see spicules projecting from them.
3. Acne rosacea: There is an erythematous, acneiform popular eruption
on the flush areas of the face or facial convexities cheeks. The
erythema is marked, with prominent dilated blood vessels
(telenhectasia). There are pustules within the eruption. Rosacea
may not spare the nasolabial folds and its pustules are characteristic.
The rash of SLE and DLE spares the nasolabial folds and pustules
are not a feature. Scarring, follicular plugging and scarring are
features of DLE but not rosacea. Acne rosacea tends to affect
females more than males, with precipitating factors including heat,
sun, alcohol, spicy foods, emotion/embarrassment, and steroids.
There is episodic flushing with erythema, telengectasia and
papules/pastules in the earlier stages. Later there is sebaceous
hyperplasia, but seborrhoea and comedones are not a feature.
Rosacea is usually symmetrical. Steroids should not be used. They
are not effective in the long term and tend to cause skin addiction
and rebound flares. Avoidance of precipitating factors is seldom
helpful except for the use of sunscreens. Topical treatments included
4.
5.
6.
7.
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metronidazole or erythromycin gel, with an emollient. Systemic

treatments include oral tetracycline, minocycline, and doxycycline.
Isotretinoin is usually beneficial. Rhinophyma occurs in later cases.
[NB. Acne vulgaris causes comedones without telengectasia, and
its distribution is generally wide. It is a chronic inflammatory
disorder of the pilosebaceous structure, characterized by
comedones (non-infmaled lesions), erythematous papules, pustules
and nodules (inflamed lesions), and scarring. Scarring tends to be
hypertrophic and keloid (trunk) or ice pick.]
Lupus pernio: These are purple/red/violaceous plaques on the nose,
cheeks and earlobes with telengiectasia over and around the
plaques. The plaques have a yellowish translucency. They tend to
flatten with time. Lupus pernio and lupus vulgaris are not pustular.
Lupus vulgaris: This is the skin manifestation of tuberculosis and is
rare in the UK. The lesion has an apple jelly consistency when a
translucent slide is rested upon it.
Dermatomyositis: There is a heliotrope rash around the eyelids. It
may also affect the malar region, limb extensors, knuckles and
trunk. Gottrons papules may be present on the dorsum of the
hands (notably metacarpophalangeal joints and interphalangeal
joints), and occasionally elsewhere. Nailfold erythema due to
dilated capillaries is often present, and the cuticles may be ragged.
Seborrhoeic dermatitis
BULLOUS DISORDERS
Pemphigus: Lesions in mouth common. Autoantibodies against
desmosomes which bridge adjacent epidermal cells. Bullae tend to
break easily and even rubbing of normal skin causes sloughing of the
epidermis (Nikolsky sign). Widespread crusting and erosions. Bullous
eruption on the trunk and flexor surfaces. Treat with steroids and
immunomodulatory drugs.
Pemphigoid: Mucosal ulceration rare. Autoantibodies present at the
dermo-epidermal border. Tense bullae present with erythematous
plaques. Many burst, leaving red, exuding, tender patches. Tends to
affect the elderly. Treat with steroids.
ERYTHEMA NODOSUM
[See also painful shins under the History taking chapter (Chapter 4).]
Key signs are flat, red, tender, nodular large lesions on the shins,
associated with fever and arthralgia.

Signs of a cause, e.g. red, sore throat or systemic manifestations of
sarcoidosis. Investigations: History, may be due to sarcoid, check ACE
and CXR, TB.
Causes of erythema nodosum include streptococcus, salmonella
or campylobacter gastroenteritis; sarcoidosis; tuberculosis; oral
contraceptive pill, sulphonamides, tetracyclines, penicillin; ulcerative
colitis, Crohns disease; lymphoma/malignancy; viral/chlamydial
infection; pregnancy.
Management: Often self-resolving, treat sarcoid if required, or
remove cause. Other skin manifestations of sarcoidosis: Nodules and
plaques (red/brown seen particularly around the face, nose, ears and
neck. Demonstrates Koebners phenomenon) and lupus pernio (bluish/
brown plaque with central small papules commonly affecting the nose).
PYODERMA GANGRENOSUM
This may begin as a nodular erythema or a sterile pustule, but develops
often into large areas of painful, necrotic ulceration. There are large
necrotic ulcers with ragged bluish-red overhanging edges together
with areas containing erythematous plaques with pustules. They are
situated on the legs. The appearances are suggestive of pyoderma
gangrenosum. The patient may have Crohns disease or ulcerative
colitis.
Other causes: Gastrointestinal (ulcerative colitis, Crohns disease),
rheumatological (rheumatoid disease, ankylosing spondylitis), liver
(chronic active hepatitis, primary biliary cirrhosis, sclerosing
cholangitis),
haematological
(lymphoproliferative
and
myeloproliferative disorders), others (diabetes mellitus, thyroid
disease, sarcoidosis, Wegeners disease).
It is frequently an indicator of severity of the disease. Systemic
steroids often help. The adjunctive use of minocycline may reduce
corticosteroid requirements. Other causes of leg ulcers include venous
ulceration, ischaemic arterial ulceration, diabetes mellitus, vasculitis,
infection, Charcots joints, tumour, haematological (sickle cell,
thalassaemia, pnh), neurological (diabetes, tabes dorsalis, leprosy,
syringomyelia).
LEG OEDEMA
In bilateral oedema look for:
Signs of right heart failure, especially raised jugular venous
pressure.
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Involvement of the face/periorbital tissues suggesting nephrotic

syndrome.
Signs of chronic liver disease (hypoalbuminaemia may occur, look
for leuconychia).
Palpate inguinal nodes for enlargement; malignant infiltration may
occur causing secondary lymphoedema.
Comment on the desirability of abdominal, rectal and vaginal
examination to exclude malignancy.
In unilateral oedema look for:
Other signs of deep vein thrombosis.
Measure the calf with a tape measure.
Consider ruptured Bakers cyst, especially in a patient with
osteoarthritis or rheumatoid arthritis. Ultrasound, arthrography
and/or venography may be necessary to distinguish between the
two conditions.
Look for varicose veins, venous eczema and ulceration.
NECROBIOSIS LIPOIDICA DIABETICORUM

A common spot case.
Associated with diabetes in about 75% of cases.
Histology: Collagen degeneration with surrounding epithelioid and
giant cells.
Well-demarcated plaques with waxy-yellow centre and red-brown
edges, coalescing oval plaques on the shins. The lesions have a shiny
atrophic surface and may ulcerate. Prominent skin blood vessels.
Treatment: Topical steroid and support bandaging. Tight glycaemic
control does not help, but this should be tried. Steroids administered
cautiously may help. The histology varies, some containing large
amounts of lipid.
OTHER DIABETIC CHANGES

Cheirarthropathy: Tight waxy skin that limits finger extension.
Granuloma annulare: Flesh-coloured papules in annular configurations
on the dorsum of the fingers. These are pale or flesh-coloured papule
coalescing in rings of usually 1-3 cm diameter, especially on the backs
of the hands and fingers. Blanching by pressure reveals a characteristic
beaded ring of white dermal patches. It is sometimes associated with
diabetes especially when the lesions are generalized and atypical.
LIPIDS
Details, cardiovascular history, diabetes history, hypertension history,
family history of ischaemic heart disease, alcohol, smoking, dietary
and exercise history, concerns of patient. Need to minimize risk factors
related to the above, multidisciplinary team including dietitian, statins.
Proteinuria and hypertension 24-hour urinary collection, ACEinhibitor, angiotensin-II receptor antagonist.
Hypercholesterolaemia: Tendon xanthomata, xanthelasma and corneal
arcus.
Hypertriglyceridaemia: Eruptive xanthomata and lipaemia retinalis
Secondary hypercholesterolaemia: Hypothyroidism, nephrotic syndrome,
alcohol, cholestasis.
Extensor tendon xanthomata: Classically occur in the extensor surfaces
and may become more obvious when the patient clenches his fist. Look
also for xanthomata in the Achilles tendons and patellar tendons. Look
for xanthelasmata and corneal arcus. Aetiologiy is ischaemic heart
disease. Remember than tendon xanthomata are classically found in
Type IIA lipoproteinaemia: This may be primary (familial
hypercholesterolaemia), or secondary (seen in jaundice). Investigations
are cholesterol (markedly elevated), HDL, LDL and triglycerides, family
history.
Eruptive xanthomata are multiple red or yellow vesicles which are
found on extensor surfaces: Back, buttocks, elbows, knees. These are
not usually associated with tendon xanthomata or xanthelasmata. Ask
if you may inspect the fundi for lipaemia retinalis (found in severe
hyperlipidaemia, which is associated with diabetes mellitus and
obesity). Symptoms may be of diabetes, pancreatitis and ischaemic
heart disease. It also occurs in Types I and V lipoproteinaemia.
Findings are raised triglycerides, cholesterol may be normal. Plasma
appears lipaemic. HBA1c.
Palmar xanthomata are rare xanthomata which are orange or yellow
discolourations of the palmar and digital creases being most distinctive.
Look also for tubo-eruptive xanthomata characteristically found over
the knees and elbows. Check the eyelids for xanthelasmata, which
are also associated.
Xanthelasmata: Never forget the importance of inspection. Look for
the corneal arcus, which often coexists with xanthelasmata and is
299
typically most pronounced at the 12 and 6 oclock poitions (in contrast

to corneal calcification which tends to be maximal at the 3 and 9 oclock
positions). Look for tendon xanthomas in the hands and Achilles
tendons. Check the palms for xanthomata and tell the examiner you
would like to take the patients blood pressure and test the urine for
glucose (hypertension and diabetes mellitus being associated with
Type IIB lipoproteinaemia). Remember that xanthelasmata and corneal
arcus may occur in normal people, type IIA lipoproteinaemia, type
IIB lipoproteinaemia, type III lipoproteinaemia. Associations of
xanthelasmata also include hypothyroidism, nephrotic syndrome and
chronic obstructive jaundice.
PRETIBIAL MYXOEDEMA
Key signs: Elevated symmetrical skin lesions over the anterolateral
aspects of shin.
Coarse: Purplish red
Raised with well-defined serpiginous margins.
Skin is shiny and has an orange-skin appearance. Hairs in the
affected areas are coarse and lesions are tender.
Remember to check for thyroid acropachy.
Skin in the superficial area is infilitrated with mucopolysaccharide.
Biopsy scars then to develop keloid.
The latent interval between treatment for hyperthyroidism and
onset of pretibial myxoedema varies from 4 to 31 months with a mean
time 1 year.
SYSTEMIC SCLEROSIS
Female: Male ratio = 4:1, usual age of presentation is 40.
Key signs: Pinched cheeks, microstomia, telengectasia, look at fingers,
ask if you can check for Raynauds swallowing. Calcinosis, Raynauds
Phenomenon (white to blue to red), oesophageal involvement,
sclerodactyly and telegectasia. Morphoea (focal/generalized patches
of sclerotic skin which does not progress to systemic involvement;
characterised by thickened, waxy plaques on the trunk or limbs), en
coup de sabre (scar down central forehead).
Other organ involvement: Renal failure 20% may be associated with
accelerated hypertension responsive to ACE inhibitors, heart

(pericardial effusion), musculoskeletal, intestine (rarely hypomotility
with a dilated second part of the duodenum leads to bacterial
overgrowth). Pulmonary hypertension may develop independent of
parenchymal changes. Interstitial fibrosis (fine, bibasal crackles).
Definition: Limited is distribution limited to hands, feet and face, tight
thick skin, microstomia, CREST syndrome, slow progression (years);
diffuse is widespread cutaneous and early visceral involvement, rapid
progression (months).
Investigations: Skin biopsy, autoantibodies (ANF positive in 90%, 80%
limited anti-centromere, 70% diffuse anti-Scl 70 antibody which has
an increased association with pulmonary fibrosis), renal function (and
dipstix the urine, urine microscopy for casts, and consider renal
biopsy), pulmonary function, oesophageal motility, blood pressure,
echocardiogram and ECG primarily to assess pulmonary artery
pressures and presence of pericardial effusions. Antibody to U3
ribonucleoprotein may also occur, present mainly in parients with
diffuse disease and overlap syndromes.
Management: Supportive, topical camouflage creams, Raynauds therapy
(gloves, hand-warmers, calcium channel blockers, ACE inhibitors,
prostacyclin infusion for severe), dependent on systemic involvement
(Renal: Hypertensive control; Malabsorption: Low-residue diets,
nutritional supplements; oesophageal symptoms-proton pump
inhibitors and prokinetic drugs). Generaleducation, counselling,
family support. Contractures exercises and lubicrants.
The 5 years cumulative survival is 35-75%. Adverse factors are
increasing age, male sex, extent of skin, heart and renal involvement.
Hypertensive renal crises are an important cause of morbidity being
a 30% 10 years survival while pulmonary involvement has a 50%
survival.
LEG ULCERS
Venous: Painless ulcers, gaiter area.
Stigmata of venous hypertension: Varicose veins or scars from vein
stripping, oedema, lipodermatosclerosis, varicose eczema, atrophie
blanche.
Cause: Abdominal/pelvic mass.
Investigation: Doppler ultrasound of the venous system.
301
Treatment: Remove exudates and slough with regular cleaning with

tapwater or saline, apply liquid paraffin/white soft paraffin, treat
surrounding venous eczema, four-layer compression bandaging, vein
surgery. If infected, take swabs, but do not use topical antibiotics as
they can be sensitizers (e.g. neomycin).
Arterial: Painful, distal extremities and pressure points, trophic changes:
Hairless and paper-thin shiny skin, cold with poor capillary refill,
absent distal pulses.
Cause: Check for atrial fibrillation or cardiac murmur.
Investigation: Ankle-Brachial Pressure Index (0.81.2 is normal, <0.8
implies arterial insufficiency), arteriography.
Many patients have contact dermatitits to previous topical
treatments.
Treatment: Angioplasty, vascular reconstruction, amputation
Neuropathic: Painless, pressure areas, e.g. under metatarsal heads,
peripheral neuropathy.
Cause: Look for diabetic signs, Charcots ulcer, diabetes mellitus, tabes
dorsalis, syringomyelia.
Complications: Infection, malignant change (Marjolins ulcer).
Othere causes: Vasculitic, neoplastic, infectious, haematological, tropical.
PIGMENTARY CHANGES
Hyperpigmentation
Causes of hyperpigmentation include:
Genetic (Peutz-Jehgers syndrome; xeroderma pigmentosum;
Albrights syndrome).
Metabolic (cirrhosis, haemochromatosis, porphyria, renal failure).
Drugs (oral contraceptive pill, minocycline, amiodarone).
Endocrine (Addisons disease, Cushings syndrome, Nelsons
syndrome, pregnancy).
Nutritional (malabsorption, carcinomatosis, Kwashiokor, pellagra).
Post-inflammatory (lichen planus, eczema, secondary syphilis and
cutaneous amyloid).
Hypopigmentation
Causes of hypopigmentation include:
Genetic (albinism, phenylketonuria, tuberous sclerosis).
Chemical (chloroquine).
Infections (pityriasis versicolor).
Endocrine (hypopituitarism).
Autoimmune (vitiligo).
Post-inflammatory (eczema, psorias, lupus erythematosus).
ALOPECIA
Distribution: Look for hair loss on the body and signs of anaemia,
thyroid disease, autoimmune or skin disease. Check for features of
androgen excess in females e.g. acne, hirsutism, virilization. Dont
forget to look at the nails too (e.g. lichen planus, alopecia areata,
Beaus line in telogen effluvium).
Table 8.1: Types of alopecia
Scarring (usually patchy)
Discoid lupus erythematosus

Lichen planus
Cicatrial pemphigoid
Sarcoidosis
Tumours, e.g. BCC
Burns
Radiation
Infections including fungal kerion
Traction (late changes)
Non-scarring and patchy
Androgenetic alopecia
Alopecia areata
Tinea capitis
Traction (in early stages)
Secondary syphilis
Non-scarring and generalized

Iron deficiency
Telogen and androgen effluvium
Drugs
Alopecia totalis
Endocrine, e.g. thyroid disease
Hypopituitarism
Malnutrition
SLE
Chronic disease
Alopecia areata may resolve with no treatment or may fail to

resolve with maimum treatment. Topical or locally injected steroids
may be used; short systemic course have poor evidence of sustained
benefit.
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ACANTHOSIS NIGRICANS
Brown velvet-like skin change commonly found in the axillae.
Associations: Obesity, cultural, type II diabetes mellitus, acromegaly,
malignancy, e.g. gastric carcinoma and lymphoma.
PSEUDOXANTHOMA ELASTICUM
Plucked chicken skin appearance: Loose skin folds especially at the
neck and axillae, with yellow pseudoxanthomatous plaques.
Hyperextensive joints.
Extra points: Blue sclerae, reduced visual acuity, hypothyroidism,
miscarriages, retinal angioid streaks and macular degeneration.
Cardiovascular: Blood pressure 50% are hypertensive, mitral valve
prolapse, CVA and/or CCF from atherosclerosis, peripheral vascular
disease.
Discussion: Inheritance: Autosomal dominant or recessive,
degenerative elastic fibres in skin, blood vessels and eye, premature
coronary artery disease.
TUBEROUS SCLEROSIS
There is a papular, salmon-coloured eruption on the centre of the
face, especially the nasolabial folds. These angiomatous glistening
papules and their configuration have the appearance of adenoma
sebaceum (look for periungual fibromata and shagreen patches). There
may be a history of epilepsy and mental deficiency which together
with adenoma sebaceum make up tuberous sclerosis. Other organs
affected are the cerebral hemispheres (multiple hamartomata or
tubers), renal hamartoma in 2/3 of paients, retinal hamartoma which
appear yellow, cardiac hamartoma, and cystic lung disease.
EHLER-DANLOS SYNDROME
Early scarring, fish mouth scars especially on the knees. No skin
folds.
Fragile skin: Multiple ecchymoses.
Hyperextensible skin: Able to tent up skin when pulled (avoid doing
this)
Joint hypermobility and dislocation.

Extra points: Mitral valve prolapse, abdominal scars (aneurismal rupture
and dissection, bowel perforation and bleeding).
Discussion: Autosomal dominant, defect in collagen increasing skin
elasticity, no premature coronary artery disease.
HEREDITARY HAEMORRHAGIC TELANGECTASIA/

OSLER-WEBER-RENDU
Small, flattened multiple telengectasia on the face, lips and buccal
mucosa.
Anaemia: Gastrointestinal bleeding.
There may be clubbing due to aneurysms/AV malformations in the
lung.
Examine the respiratory system, particularly for cyanosis and a
chest bruit, and a pulmonary vascular abnormality/shunt. Their
presence can result in complications such as pulmonary haemorrhage;
they may be sufficiently large or numerous to cause shunting (right
to left) with resultant hyoxia, and, additionally, they may be involved
in paradoxical embolic events.
Discussion: Autosomal dominant, increased risk of gastrointestinal
haemorrhage, epistaxis and haemoptysis.
Vascular malformations: Pulmonary shunts, intracranial aneurysms
(subarachnoid haemorrhage).
EXFOLIATIVE DERMATITIS
Exfoliative dermatitis may occur in response to drug therapy, systemic
disease or an idiopathic entity. Common causes are systemic disease
(lymphoma, leukaemia, multiple myeloma, carcinoma of the lung,
prostate, colon and thyroid, immunodeficiency, Hodgkins disease),
cutaneous diseases such as psoriasis, seborrhoeic dermatitis, atopic
dermatitis, Mycosis fungoides and lichen planus, and drugs such as
codeine, captopril, antimicrobials such as cephalosporins, and
barbiturates. Laboratory studies include serum albumin, ESR, and
investigation of cardiac, renal and intestinal failure. General measures
are to withdraw implicated medications and identify underlying
infection and/or disease, protect the patient from the development
of hypothermia, advise local moisturizing ointments, advise highprotein diet with folic acid supplementation since protein losses can
be high, and urgent dermatological referral. Complications include
hypothermia, superinfection, dehydration and heart failure.
305
SKIN MALIGNANCY
Basal cell carcinoma: Usually on the face/trunk, sun-exposed areas,
pearly nodule with rolled edge, superficial telengectasia, ulceration
in advanced lesions, local invasion and distant metastasis, other
lesions.
Natural history: Slowly grow over a few months, local invasion only,
rarely metastasize.
Treatment: Curettage/cryotherapy if superficial, surgical excision +
radiotherapy.
Squamous cell carcinoma: Sun-exposed areas (+ lips + mouth), actinic
keratoses (pre-malignant, red-scaly patches), varied appearance
(keratotic nodule, polypoid mass, cutaneous ulcer), local invasion and
distant metastasis, other lesions.
Management: Biopsy suspicious lesions, surgery + radiotherapy, 5%
metastasize.
Malignant melanoma: Clinical risk factors (light hair, blue eyes),
asymmetrical, border irregularity, color (black often irregular
pigmentation), diameter > 6 mm. Local invasion and distant metastasis,
other lesions.
Management: Excision, staged on Breslow thickness (maximal depth
of tumour invasion into dermis), < 1.5 mm = 90% 5-year survival, >
3.5 mm = 40% 5-year survival.
POLYMYOSITIS AND DERMATOMYOSITIS

Heliotrope rash around the eyes. Gottrens papules on the MCP joints.
Proximal muscle weakness and wasting with muscle tendereness.
Diffuse calcification within the muscles.
40% of patients have primary disease with unknown aetiology.
Associated with malignancy in 10-25% of cases, especially lung
and ovary.
Look for clubbing, Horners syndrome, lymphadenopathy or
hepatomegaly.
It is associated with other autoimmune disorders in 10% of cases,
e.g. rheumatoid arthritis, SLE.
Juvenile forms are associated with contractures and calcification
of muscle.
Symptoms: Muscle pain and weakness, dysphagia and symptoms of
the cause.

Investigations: CK, aldolase, LDH, EMG small polyphasic potentials,
spontaneous; muscle biopsy inflammatory cell infiltrates with muscle
necrosis; tumour markers, e.g. CA125, CEA.
Autoimmune profile (ANA weakly positive in 60-70%, anti-Jo-1 is
specific).
Respiratory Function Tests

Treatment: Supportive, physiotherapy, exercise, immunosuppressants
(high-dose steroids and azathioprine if steroid-unresponsive, 20% of
patients recover fully).
Consider malignancy, if male > 45 years of age; absent
autoantibodies; poor response to treatment.
LIVEDO RETICULARIS
There tends to present as an arborescent pattern of reddish-blue
erythema (or pigmentary change), and may be associated with
antiphospholipid antibody syndrome, collagen vascular disease
especially polyarteritis nodosa, cryoglobulinaemia or a hyperviscosity
syndrome. APAS is a hypercoaguable condition leading to both venous
and arterial occlusions. Lupus anticoagulant and anticardiolipin
antibodies are the serological markers. DVT, transient ischaemic attack,
cerebrovascular attack, migraine, epilepsy and recurrent abortions
may all be manifestations. APAS is also being recognised as a primary
condition.
LICHEN PLANUS
This presents as an itchy, violaceous, flat-topped, polygonal, popular
rash with white lines on the surface called Wickhams striae. Other
affected sites include mucous membranes, genitalia, palms, soles, scalp
and nails. On the buccal mucosa, it causes a white lace-like pattern.
Causes of white lesions in the oral mucosa include: Leucoplakia, chronic
candidiasis, and chemical burns.
LOCOMOTOR
Examine the joints of (a certain part of the body) and discuss with the
examiners.
GENERAL LOCOMOTOR SCREENING GALS

Joint appearance: Swelling, deformity, restricted movement.
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Muscle wasting: Global and localised wasting, specific muscles or

groups.
Function with relation to activities of daily living.
Look, feel, move algorithm.
Inflammatory arthritis compared to non-inflammatory arthritis.
A specific system, often used in short cases is GALS: Gait (look
for any symmetry, deformity in leg length, spinal curvature, arm
swing), Arms, Legs, Spine (see below).
Ask with some screening questions:
Have you any pain or stiffness in your arms, legs or back?
Can you walk up and down stairs without difficulties?
Can you dress yourself in everyday clothes without any help?
Gait
You may be asked to describe the gait of a patient with hip pathology.
The two main types are antalgic and the Trendelenburg gait.
Table 8.2: Differences between an antalgic gait and a Trendelenburg gait
Cause
Antalgic gait
Trendelenburg gait
Painful hip
Inefficient hip abduction
Weight-bearing/stance phase
opposite side
Shortened
Pelvis droops on the
Direction to which body

Towards affected side Towards unaffected side
leans whilst weight-bearing
You may be asked to describe the mechanism of the Trendelenburg

gait. Normally, when standing on one leg, the abductors on the weightbearing side contract so that the pelvis rises on the opposite side. A
positive Trendelenburg test occurs when there is any inefficiency of hip
abduction: The pelvis droops towards the unsupported side.
Figure 8.1: Trendelenburg test

Inefficiency of hip abduction occurs as a result of the following:
disturbance in the pivotal mechanism (dislocation or sublaxation of the
hip, shortening of the femoral neck) and weakness of the hip abductors
(gluteus medius and minimus) (myopathy, usually bilateral, and
neuropathy L5 lesion, usually unilateral).
Arms
During the general inspection, you should inspect for abnormalities
such as a swelling or deformity, and look for any skin changes which
may be associated with arthritis, for example, digital vasculitis in SLE,
or evidence of peripheral infarcts from Raynauds phenomenon.
Ask the patient to show you his/her hands, palms down, and then
turn them over this is an assessment of the radioulnar joint, which is
a common site for rheumatoid arthritis. Remember to keep the elbows
tucked in, or patients can use their shoulders to perform this
movement.
Ask the patient to make a tight fist with each hand; this is a position
of function of the hands, and you can also assess power grip.
Ask the patient to place the tip of each finger onto the tip of the
thumb in turn; this permits an assessment of the dexterity and fine
finger movements of the hand which is limited in rheumatoid arthritis.
Squeeze across from the second to the fifth metacarpals; this is an
assessment of joint tenderness. Tenderness across the
metacarpophalangeal joints is a sign of rheumatoid arthritis.
Next, ask the patient to put his/her hands behind the head, pressing
the shoulders right back; this is an assessment of abduction and external
rotation of the shoulder with flexion of the elbow. It is a measurement
of shoulder and elbow movement as well of function; it is not possible
to put on a tie or comb your hair unless you can do this manoeuvre.
Look for any shoulder pain (observe shoulders for asymmetry
and swelling; palpate the capsule over the anterior humeral head and
the supraspinatus tendon over the lateral upper humerus for
tenderness; assess flexion, extension, abduction, adduction, internal
and external rotation both actively and passively).
Legs
Ask the patient to lie back on the couch and flex the hip and knee
while holding the knee. Ensure normal knee flexion, feel for crepitus,
and also test hip flexion.
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Then passively and internally rotate the hip with the knee and hip
still flexed; this is a measurement of knee movement and internal
rotation of the hip.
Look for any hip pain (look for flexion deformity of the hip; assess
flexion at the hip with the knee flexed to relax the hamstrings; assess
internal and external rotation in flexion).
Look for any knee pain (look at the quadriceps muscle, wasted in
significant knee disease; look for selling and perform the bulge test;
flex and extend the knee to its fullest extent in either direction).
Ask the patient to flex, extent, invert, and evert the ankle in order
to assess tibiotalar (affected by osteoarthritis) and subtalar (affected
by inflammatory arthritis) movements.
Squeeze the metatarsals, again looking for rheumatoid arthritis,
in the same way as looking over the metacarpals.
Spine
Observe the curvature of the cervical and thoracic spine in the posterior
and lateral plane.
Ask the patient to stand up and put his/her ear to each shoulder
in turn; this is an assessment of lateral fusion of the neck, which is lost
with either osteoarthritis or rheumatoid arthritis affecting the neck.
Put two fingers over adjacent spinous processes in the lumbar
region, and then ask the patient to bend over and touch his/her toes;
your fingers should move apart. This is a modification of a Scrobers
test which is designed to pick up a lack of movement associated with
ankylosing spondylitis.
Ensure the pelvis is symmetrical/no abnormal rotation.
Look for low back pain (assess the curvature of the spine, palpate
the erector spinae muscles to assess spasm, perform a Modified
Schrobers test, ask the patient to lean over to each side in turn, ask
the patient to lean over backards to assess extension, passively flex
the hip keeping the knee extended and then passively dorsiflex the
ankle this is the sacral stretch test, and is positive if the patient
complains of any sensory disturbance below the knee; the counterpart
to this is the femoral stretch test by passively flexing the knee and
extending the hip a positive test is irritation over the front of the
thigh).
MONOARTHRITIS
Table 8.3: Types of monoarthritis
Infective/trauma
Septic arthritis
Gonococcal or meningococcal infection
Rheumatic fever
Viral infections
Seronegative arthropathies
Reiters disease
Reactive arthropathy
Ankylosing spondylitis
Psoriatic arthropathy
Enteropathic arthropathy
Metabolic
Gout
Pseudogout (associated with hyperparathyroidism,
hyperuricaemia and gout, haemochromatosis, acromegaly,
diabetes mellitus, renal failure, Wilsons disease, ochronosis)
Haematological
Haemophilia
Sickle cell anaemia
Other
Osteoarthritis
Rheumatoid disease
When discussing your management, always mention the

importance of aspiration of the joint and culture of the fluid for
bacterial infection/microscopy for crystals.
POLYARTHRITIS
Rheumatoid arthritis
Osteoarthritis
Gout/pseudogout
SLE
Polyarteritis nodsa
Rheumatic fever
Ankylosing spondylitis
Reiters disease/reactive arthritis
Psoriasis
Stills disease
Sarcoidosis
Infective endocarditis
Others: Systemic sclerosis, Whipples disease, Behcets disease,
alkaptonuria.
Tests: Rheumatoid factor, ANA, HLA typing.
CHARCOTS JOINT
Painless deformity and destruction of a joint with new bone formation
following repeated minor trauma secondary to loss of pain and
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sensation. The most important causes are tabes dorsalis: hip and knee,
Diabetes: Ankle, syringomyelia: Elbow and shoulder. Treatment:
Bisphosphonates can help.
PSORIATIC ARTHROPATHY
Psoriatic arthropathy affects up to 10% of patients with psoriasis and
may proceed or follow skin disease by months or even years. There
are in theory five types although overlapping pictures are common.
Types of psoriasis: Pustular psoriasis, guttate psoriasis, flexural psoriasis,
erythrodermic psoriasis.
Asymmetrical distal interphalangeal joint arthropathy. This is
relatively uncommon but the form most strongly associated with
psoriasis. Affected digits often show nail changes such as pitting.
This is an oligo- or monoarthritis.
Rheumatoid like hands. This is the commonest arthropathy and is
seronegative. Exclude rheumatoid nodules at the elbows and look
for psoriatic changes. Predominantly affects DIP joints.
Asymmetric large joint mono- or oligo-arthropathy. Tell the
examiners you would ask about large joint pain or swelling.
Spondyloarthropathy or sacroiliitis. Tell the examiners you would
ask about low back pain. Appears like anykylosing spondylitis.
Arthritis mutilans: A very uncommon, severely destructive form.
Tests: Skin biopsy, skin scrapings and nail clippings to rule out tinea,
X-ray of the affected joints pencil-in-cup deformity, RA factor.
Treatment: Emollients, coal tar, short acting dithranol, talcacitol,
steroids used topically, narrow band UVB phototherapy, retinoic acid
derivatives, methotrexate in severe refractory disease/severe
erythrodermic form/arthropathy, NSAIDs for arthropathy, and scalp
psoriasis.
Sulphalazine and methotrexate are becoming established as
treatment for psoriatic arthropathy. Ciclosporin may have a place in
refractory disease.
RHEUMATOID DISEASE
Symmetrical, deforming arthropathy.
Signs
1. Joints: Typically a distal, symmetrical, small joint polyarthritis
involving the proximal interphalangeal joint and
metacarpophalangeal joints of the hand, wrist, metatarsophalangeal
joints, ankles, knees and cervical spine.
2. Upper limbs: Soft tissue swelling around affected joints, spindleshaped appearance of the fingers, trigger fingers due to
tenosynovitis of the long finger tendons, compression of the Median
nerve, Tinels sign and Phalens sign. Volar sublaxation of the
metatarsocarpophalangeal joints, ulnar deviation and sublaxation
of the fingers. Swan neck deformity. Boutonniere (button-hole)
deformity and Z deformity of the thumb. Piano-key sign. Distal
ulna migrates dorsally which can be depressed by pressure like a
piano key. Subcutaneous nodules are commonly found on the
extensor surface of the forearm of the elbow. Wasting of small
muscles of the hand, use restricted by weakness, deformity and
pain. Palmar erythema. Elbow and shoulder disease.
3. Lower limbs: Synovitis of the metatarosphalangeal joints resulting
in larger shoe size. Valgus deformity of the hindfoot is normal
and valgus deformity of the knee at a later stage.
4. Extra-articular manifestations: Rheumatoid nodules (subcutaneous
and intracutaneous nodules), anaemia (moderate anaemia
invariably), lung involvement (pleurisy, nodules and pulmonary
fibrosis), cardiac (pericardial effusion), vasculitis (aortic valve more
than mitral valve), Eye (Sjogrens syndrome, Episcleritis, Scleritis),
peripheral nerve involvement (entrapment neuropathy), muscle
(reflex inhibition and wasting resulting from severe joint pain),
liver (hepatosplenomegaly), Feltys syndrome (splenomegaly + RA
+ leucopenia).
Assess disease activity: Red, swollen, hot, painful hands imply active
disease.
Assess function: Power grip squeeze my fingers, precision grip pick
up a coin, key grip pretend to use this key, remember the
wheelchair, walking aids and splints.
Extra points: Exclude psoriatic arthropathy (main differential), nail
changes, Psoriasis: Elbows, behind ears, scalp, and around the
umbilicus.
Surgical scars: Carpal tunnel release (wrist), joint replacement (especially
thumb), tendon transfer (dorsum of the hand); steroid side effects;
C-spine stabilization scars; systemic manifestations.
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Causes of anaemia in rheumatoid disease: Anaemia of chronic disease, GI

bleeding due to NSAIDs, bone marrow suppression (gold,
indomethacin, methotrexate, penicillamine, sulphalasine),
megaloblastic anaemia, Feltys syndrome.
Systemic manifestations: Pulmonary (pleural effusions, fibrosing
alveolitis, obliterative bronchiolitis, Caplans nodules), eyes (secondary
Sjogrens, scleritis), neurological (carpal tunnel syndrome, atlantoaxial sublaxation, peripheral neuropathy), haematological (Feltys
syndrome, all types of anaemia), pericarditis.
Investigations: Elevated inflammatory markers, radiological changes
(soft tissue swelling, loss of joint space, articular erosions, periarticular
osteoporosis), positive rheumatoid factor in 80%. The presence of
nodules clinically means that the disease is seropositive.
Management: Medications: First-line. NSAIDs, oral, daily. COX-2 (e.g.
celecoxib, rofecoxib, meloxicam) inhibitors had been recommended
by NICE for those people with rheumatoid arthritis or osteoarthritis
who are at high risk of developing serious gastrointestinal problems,
but have been discontinued due to adverse effects.
Second line: Disease modifying drugs. Gold salts. D-penicillamine,
antimalarials (hydroxychloroquine) and sulphalazine.
Third line: Cytotoxic drugs and corticosteroids. Steroids are still
commonly used, as background therapy or large oral pulses. They
are also used as intra-articular injections into inflamed joints. I/m
injection as flare-up. Azathioprine, cyclophosphamide, chlormabucil
and methotrexate, anti-tumour necrosis factors (e.g. infliximab/
etanercept). Some trials show dramatic improvement in symptoms
and apparent halting of disease progression. Early treatment is critical.
Methotrexate is a medication where alcohol consumption should
ideally not exceed eight units per week.
Surgery: Soft tissue procedures, repair of ruptured tendons, tendon
transfers, decompression and transfer of nerves, synovectomy,
arthrodesis, joint replacement arthrodesis.
Life-style modification: Splinting of affected joints, gentle massage, local
heat or cold application, regular exercise.
Explanation and education (patient, carer)
Dietary advice (weight reduction, fish oil, fish supplements,
primrose oil).

Side effects of NSAIDs: Renal, neurological (uncommon), dermatological
(rare, erythema multiforme), haematological (aplastic anaemia),
hepatitis, systemic anaphylactoid reactions.
OSTEOARTHRITIS
Elderly patient + walking stick.
Asymmetrical distal interphalangeal joint deformity with
Heberdens nodes (and sometimes Bouchards nodes at the proximal
interphalangeal joint).
Disuse atrophy of hand muscles.
Crepitation, reduced movement and function.
Carpal tunnel syndrome, reduced movement and function.
Extra points: Carpal tunnel syndrome or scars.
Other joint involvement and joint replacement scars.
Prevalence: 20% (common)
Radiographic features: Loss of joint space, osteophytes, peri-articular
sclerosis and cysts.
Investigations: In the hand none essential, if there is involvement of
the hip, knee X-ray.
Complications: Pain, deformity, ankylosis, entrapment of nerves,
cervical spondylosis.
Treatment: Simple analgesia, weight reduction (if OA affects weight
bearing joint), physiotherapy and occupational therapy, joint
replacement, exercise for hip, knees, surgery for major joints.
ANKYLOSING SPONDYLITIS
Common symptom: Difficulty in bending down to tie shoelaces.
Key signs: Males more often than females, pain worse on waking, eased
with exercise; progression loss of spinal movements, kyphosis later
on, reduced thoracic expansion. Stooped question-mark posture,
buttock atrophy, protuberant abdomen due to diaphragmatic
breathing, reduced chest expansion (< 5 cm increase in girth), increased
occiput-wall distance (> 5 cm), Schobers Test (two points marked 15
cm apart on the dorsal spine expand by less than 5 cm on maximum
forward flexion).
Features
Iritis 30% (acute, deep aching pain, redness, photophobia, miosis,
sluggish papillary reflex).
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Aortitis 4% (Collapsing pulse and early diastolic murmur of aortic

incompetence).
Anterior uveitis.
Aortic regurgitation (4%) I would like to listen to the aortic valve.
Apical fibrosis rare (apical inspiratory crackles; probably
secondary to diminished apical ventilation).
Cardiac conduction defects 10% (usually atrio-ventricular nodal
block; other cardiac abnormalities may occur).
Neurological (atlantoaxial dislocation).
Secondary amyloidosis.
Anaemia of chronic disease.
IgA nephropathy.
Spinal fracture, cauda equina syndrome, pulmonary mycetoma
secondary to apical fibrosis and cavitation are potential complications,
as are those related to therapy, i.e. use of NSAIDs may result in GI
haemorrhage, and previous use of deep X-ray treatment led to
increased episodes of leukaemia and renal obstructive problems.
Tests: ESR, plasma viscosity, CRP (elevated), FBC (a mild
normochromic, normocytic anaemia in an untreated patient), X-ray
of the sacroiliac joints, lumbar, thoracic and cervical spine. The
radiological findings are characteristic, although their specificity
depends on the stage of the disease. Radiologically there is bilateral
sacroiliac joint involvement, with blurring the cortical margins of the
subchondral bone, followed by erosion and sclerosis. End-stage
involvement is that of ankylosis and obliteration of the joints.
Vertebral involvement starts in the lumbar region, with erosisons
and sclerosis producing a squaring of the vertebral bodies. Subsequent
involvement of the annulus fibrosis leads to syndesmophye formation
and eventual ankylosis of the spine.
90% association with HLA B27.
Management: Physiotherapy (exercise is of paramount importance,
attendance to posture throughout the day and night is essential,
hydrotherapy and physiotherapy are needed as an initial introduction
to a lifelong exercise programme), NSAIDs (needed by around 80%
of patients), anti-tumour necrosis factor medications now licensed
for this indication.
GOUT
Typically an asymmetrical polyarthropathy.

Key signs: Acute gout would be unusual in the exam, look for gouty
tophi of helix of ear and elbow, remember to look at the ears for
tophi. Asymmetrical swelling of the small joints of the hand and feet.
Joint deformity.
Cause: Urate excess. Secondary hyperuricaemia may occur in drugs
diuretics (thiazides), ethambutol, nicotinic acid; myeloproliferative
and lymphoproliferative disease (e.g. PRV, CML); chronic renal failure;
alcoholism; obesity.
Differential diagnosis: Septic arthritis, pseudogout, rheumatoid arthritis.
Investigation: Aspirate acute joints and look for crystals, negative
birefringent crystals for gout and pyrophosphate for pseudogout;
serum urate is normal or raised. FBC, U&E, serum uric acid, urinary
urate excretion.
Radology: Characteristic periarticular erosions without surrounding
osteoporosis; soft-tissue swelling.
Management: Weight reduction, alcohol and protein intake reduced,
stop drugs that make it worselow dose aspirin/thiazides, increase
hydration, high fluid intake, NSAIDs for acute episodes; intra-articular
injection of a corticosteroid may be used if necessary. NSAIDs should
be avoided in patients with renal insufficiencycolcichines if not
tolerated, and allopurinol. Long-term treatment is recommended if
there are recurrent attacks, evidence of tophi or gouty arthritis, there
is associated renal disease, the patient is young with a high serum
uric acid, and normal levels of serum uric acid cannot be achieved by
lifestyle modification.
Non-pharmacological management of gout.
Chronic tophaceous gout: Asymmetrical swelling of the small joints of
the hands and feet (commonly first MTP), gouty tophi around the
joints, ear and tendons. Reduced movement and function.
Associaions: Urate stones (nephrectomy scars).
Cause: Drug card (diuretics), lymphadenopathy (lymphoproliferative
disorder), chronic renal failure (fistulae).
DIABETIC FOOT
Ulcer, callous formation, concavity of the transverse arch lost, feet
cold, foot pulses not palpable, loss of hair. Factors which may
317
contribute to the production of diabetic foot lesions: Injury,

neuropathy, trivial injury is not noticed; consequent formation of
callosities at repeatedly traumatized pressure points; small vessel
disease; large vessel disease producing ischaemia and gangrene of
the foot; increased susceptibility to infection.
ENDOCRINE
Pituitary
ACROMEGALY
This 52-year-old man has had tingling in his hands. What is the
endocrine diagnosis?

Important clinical signs: Prominent supraorbital ridges, prognathism
(protrusion of lower jaw), soft tissue enlargement of the nose and
ears, macroglossia with thick lips, thick skin with hypertrichosis, spadelike hand, broad toes, acanthosis nigricans. Broad nose. Sweaty skin:
Interdentular spaces are increased. Cranial nerve involvement in
acromegaly: Bitemporal hemianopia, optic atrophyaffection of the optic
nerve, external ophthalmoplegia and deafness; Metabolic features:
Diabetes and hypertension. Coarsening of features. Voice may be
husky. Other features: Heart failure, hirsuite, hypopituitary, kyphosis,
lactation, myopathy (proximal), multinodular goitre in 10-20%.
Paraesthesia may be due to carpal tunnel syndrome or a peripheral
neuropathy secondary to diabetes mellitus.
Ask the patient if any member of he family has noticed any change
in facial appearance, whether there has been any recent changes in
the size of clothes, gloves or shoes, whether her/she suffers from
headaches, whether there has been any sweating, and whether there
has been any problems with sweating.
The scar of previous neurosurgery is often difficult to detect, and
sometimes observed only on the gum line. Carpal tunnel scars can
also be difficult to observe.
Measures of severity: (a) Blood pressure, (b) Diabetes, (c) Bitemporal
hemianopia, (d) Carpal tunnel syndrome, (e) Obstructive sleep apnoea
(f) Colorectal cancer risk. Acromegaly develops insidiously and newly
diagnosed patients often have symptoms for years.

Signs of activity: Tight rings of hands, sweaty, headaches.
Aetiology: 99% of cases are due to a pituitary growth-hormonesecreting. adenoma; 5% of patients have MEN-1 syndrome; very
rarely, ectopic GHRH secreted from neuroendocrine carcinoid tumour.
Investigations include CXR (cardiomegaly), ECG (ischaemia), blood
pressure, baseline prolactin, testosterone, LH and thyroxine levels,
plain skull X-ray to demonstrate enlargement of pituitary fossa and
thickening of skull vault, visual field test (formal Goldman perimetry),
fasting glucose, lipid profile, colonoscopy, sleep studies. The diagnosis
is confirmed by a failure of serum growth hormone to suppress below
2 mU/L in a prolonged 75 g oral glucose tolerance test and by an
elevated IGF-1. When the diagnosis is confirmed, further dynamic
tests may be needed to determine the overall function of the anterior
pituitary (e.g. insulin tolerance test, thyroid releasing hormone and
LHRH test). Consider MRI or CT of the pituitary fossa. Other features:
ECG, skin thickness, visual fields and acuity.
Management: Most patients proceed to transphenoidal surgery
(transcranial if significant suprasellar extension), by an experienced
pituitary surgeon to remove the adenoma. Cure rates of 40-90% have
been achieved. Surgery is invariably complicated by early but transient
diabetes inspidius. Larger adenomas are difficult to excise. Dopamine
agonists are generally not very effective at reducing GH secretion
and do not reduce tumour size. Somatostatin analogues such as
ocreotide can be very effective at inhibiting GH secretion, but do not
cause significant tumour shrinkage. A newly developed growthhormone receptor antagonist Pegvisomant is more efficacious,
normalising IGF-1 in > 90% of patients. External pituitary radiotherapy
alone takes several years to achieve GH reduction and often ultimately
reduced hypopituitarism and is usually for failed surgery.
Radiotherapy is given routinely post incomplete surgery to prevent
tumour recurrence and to reduce GH secretion. The greatest decrease
in growth hormone concentration occurs during the first 2-year.
Measures to reduce vascular risk factors are paramount from the
outset.
MEN (multiple endocrine neoplasia) I: Inherited tumours
(parathyroid hyperplasia, pituitary tumours, pancreatic tumours).
Causes of macroglossia: Acromegaly, amyloidosis, hypothyroidism,
Downs syndrome.
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Carpal tunnel syndrome: Thenar wasting, weakness of opposition,

abduction and flexion of the thumb, and weakness of the index finger
and middle finger lumbicals. Sensation is impaired over the palmar
aspect of the lateral side of the hand, thumb, index finger, middle
finger, and lateral radial border of the ring finger. The palm is spared
as the palmar branch of the nerve lies superior to the retinaculum.
Percussing over the medial nerve may reproduce the tingling (Tinels
sign). Flexing the wrist for 1 minute may do the same (Phalens sign).
Causes: Often idiopathic, occupational trauma, signs of rheumatoid
arthritis, gout, pregnancy, osteoarthritis, amyloid, and sometimes
there is a family history of carpal tunnel syndrome. Management: Rest,
splinting, diuretics and local hydrocortisone injection may help
temporarily while an underlying cause is relieved. Division of the
flexor retinaculum will rapidly relieve symptoms. Sensory function
will return over 6-12 months and muscle power, if impaired, may
return almost to normal.
GALACTORRHOEA
Prolactin release from the anterior pituitary is normally inhibited by
dopamine-derived from the hypothalamus.
Causes of hyperprolactinaemia are:
Physiological (stress, sleep, coitus, pregnancy/lactation)
Drugs (dopamine receptor antagonists such as metoclopromaide)
Hypothalamic or pituitary stalk disease (granulomas or
meningiomas causing disconnection hyperprolactinaemia)
Macroadenomas (e.g. acromegaly) which may secrete prolactin
Prolactinomas
Polycystic ovarian syndrome
Hypothyroidism
Idiopathic
Post seizure.
Men may present with hypogonadism causing erectile dysfunction.
KLINEFELTERS SYNDROME
This man has a testosterone patch. Why?
Revise the features of this condition. Remember that the patient
with the classical form will be tall and have eunuchoidal proportions
(span more than 5 cm greater than height; sole to symphysis pubis
greater than symphysis pubis to crown); patients are also generally
tall. The testes are small and firm. Gynaecomastia is usually present.

Axillary and facial hair will be sparse. The patient may have obesity
and varicose veins. Men are not fertile being azoospermic due to a
lack of germ cells within the testes which tend to be hyalinized.
HYPOPITUITARISM
Key signs of hypopituitarism: Cases unlikely to be in the exame but
complaing of tiredness and postural hypotension; signs include pallor,
fine facial skin, breast atrophy in females and other signs of
hypogonadism, reflecting that FSH and LH are hormones lost early.
Tell the examiners that your further assessment would include:
Decreased axillary/pubic hair.
History of brain surgery or obstetric problems.
Blood pressure measurement for postural hypotension.
Visual field assessment for bitemporal hemianopia.
Examination of the testes for hypogonadism in males.
Eliciting a history of amenorrhoea in females.
Causes of hypopituitarism are pituitary tumours, infiltration by
granulomatous disease, pituitary infarction. Diagnosis of
hypopituitarism is by combined anterior pituitary function testing,
which may include LHRH, TRH, insulin stress tests with measurement
of cortisol, growth hormone, LSH, TH, and prolactin.
Investigations: I would like to know the patients previous history. T4/
TSH. LH/FSH and testosterone for men. Short synachten test. Arginine
growth hormone releasing test.
Management: Hydrocortisone first, thyroxine, sex hormone, growth
hormone for younger patients.
ADRENOCORTICAL OVERACTIVITY (e.g. abnormalities of body
weight distribution, presence of striae, hypertension, or associated
features of Cushings syndrome or adrenal virilism).
Hyperaldosteronism may be secondary to hyperreinaemia or
primary, in which rennin levels are suppressed.
Causes of primary hyperaldosteronism include adrenal adenoma/
Conns syndrome, bilateral adrenal hyperplasia, and carcinoma.
Effects include hypokalaemic alkalosis with hypertension, especially
diastolic hypertension. Sodium is retained and extracellular fluid
volume decreases. But there is insufficient water retention for oedema.
Investigations for primary hyperaldosteronism may reveal a low
rennin level and a low ambulant or erect renin-aldosterone ratio
(screening test). Endocrine causes of hypertension are: Cushings
321
syndrome, Conns syndrome, acromegaly, phaeochromocytoma,

Liddles syndrome, glucocorticoid remediable hypertension, and
apparent mineralocorticoid excess.
Hirsutism is excessive hair growth, particularly over the face and
limbs, in androgen-dependent areas (male pattern). There may be
acne. There may be other signs of virilisation. The diagnosis of PCOS
rests on a combination of symptoms, clinical findings and biochemical
abnormalities. In addition to hirsutism, common associations are acne,
obesity, male pattern hair thinning, subfertility and oligomenorrhoea
or secondary amenorrhoea. Always consider the possibility of a
virilising adrenal tumour causing Cushings syndrome. Check for
glycosuria. Virilization refers to male pattern hair loss and other
physical changes including voice change, breast atrophy and
clitoromegaly. Hirsuitism may be constitutional, or it may be due to
adrenal or ovarian disorders, such as androgen excreting tumours in
either of these organs. It may be caused by congenital adrenal
hyperplasia. It may be caused by drugs.
CUSHINGS SYNDROME
This 42-year-old lady on the wards at present experienced some
weight gain and regularly has a bone scan. What is the endocrine
diagnosis?
Signs of corticosteroid excess. The examiners expect: Centripetal
fat distribution, truncal obesity, acne, proximal muscle wasting/
weakness (lemon on a stick appearance), cataracts, ankle oedema,
supraclavicular fat pads/moon face, thoracocervical fat pads or buffalo
lump, protein wasting, skin: thin, striae, wound healing, easy bruising,
hirsutism, oedema.
Most patients are on long-term corticosteroids for a chronic
inflammatory disease such as COPD, asthma or inflammatory bowel
disease or a retinal transplant. Rarely, pseudo-Cushings syndrome
may result from obesity, depression or sometimes alcohol excess.
Investigations: Many will be iatrogenic in the exam, Before undertaking
further tests, I would like to check that the patient is not taking
steroids for another medical problem.
Consider hypertension, glucose intolerance/diabetes mellitus.
Signs of decompensation: Osteoporosis/wedge fractures, immunosuppression, recurrent infections.
Cause: E.g. asthma, signs of RA (requiring steroids)

Diagnosis: 24-hour urinary cortisol (increased in Cushings and adrenal
tumours). Overnight dexamethosone suppression test. Low-dose
suppression test (all cases apart from pseudo-Cushings, i.e. alcohol/
depression and normal should fail to suppress). ACTH is easily
detectable in Cushings disease, and suppressed in adrenal adenoma
(secretes cortisol leading to hirsutism and virilization). Ectopic ACTH
does not suppress and is high. Circadian rhythm of cortisol secretion
is normally lost in Cushings although can be lost in stress, illness and
venepuncture.
Imaging is unsatisfactory as pituitary adenomas may be only a
few mm wide. Incidentalomas are common. CT/MRI modalities.
Treatments: Cushings disease: Transsphenoidal hypophysectomy is
the treatment of choice for proven pituitary disease, complications
being CSF rhinorrhoea, diabetes insipidus, hypopituitarism, visual
field disturbance, recurrent disease; radiotherapy; drugs such as
metyrapone; bilateral adrenalectomy if primary evacuation is not
possible (which may be complicated by Nelsons syndrome where
ACTH levels rise and cause melanin-induced hyperpigmentation).
Iatrogenic: discontinue drug. An adrenal tumour requires surgical
removal. Ectopic ACTH surgical if possible, or medical treatment,
e.g. metyrapone, aminoglutethimide, ketoconazole.
POLYCYSTIC OVARIAN SYNDROME

This 42-year-old lady, on clomiphene, was concerned about her weight
gain. What is the endocrine diagnosis?
The pathophysiology of PCOS is incompletely understood. It is a
condition of androgen excess, characterized biochemically by: Raised
testosterone and androstenedione levels, a raised LH:FSH ratio with
an abnormality in the usual pulsatile secretion of gonadotrophin
releasing hormones, normal or elevated oestradiol levels, mild
hyperprolactinaemia, low sex hormone binding globulin levels, low
HDL cholesterol.
Congenital adrenal hyperplasia are a group of disorders, all
autosomal recessively inherited, the commonest being 21-hydroxylase
deficiency. There can be a spectrum of clinical manifestations from
mild, late onset signs resembling PCOS in females, to ambiguous sexual
differentiation at birth. The enzyme defect results in a deficiency of
glucocorticoids or mineralocorticoids leading to hyperstimulation of
the adrenal gland which can only respond by producing excess
hormones from unaffected pathwaystestosterone precursors and
testosterone.
323
PRIMARY HYPOADRENALISM (e.g. weight loss, associated with

disturbance of pigmentation such as buccal pigmentation).
There is hyperpigmentation, especially of skin creases (palms,
elbows), lips and mouth, and surgical scars. There may be signs of
other autoimmune disease such as vitiligo, and sparse axillary (and
pubic) hair. There is postural hypotension. Ask about nausea and
vomiting, and weakness, fatigue and weight loss. Mention that
tachycardia would be a critical sign. Wish to know the results of serum
electrolytes (tendency to hypokalaemic, hyperchloraemic metabolic
acidosis with hyponatraemia, but results may be normal).
A short Synachten test would be the next step (teratosactrin 250
um IM), to determine whether or not administered synthetic ACTH
can stimulate an appropriate rise in cortisol levels to greater than 500
nmol/L. The diagnosis can then be confirmed by measurement of
plasma ACTH which is greatly raised. Causes of hypoadrenalism
include Addisons disease, TB, HIV, amyloid, metastatic, fungal
infiltration (histoplasmosis), adrenoleucodystrophy, WaterhouseFriederechsen syndrome.
Management: Steroid warning card, patients should be taught how to
give a IM injection in case of vomiting or coma, hydrocortisone, warn
patient about intercurrent illnesses, Medicalert bracelet,
Fludrocortisone only if high renin electrolyte problems or continuing
postural hypotension.
HYPOGONADISM
What is the endocrine diagnosis?
Testosterone deficiency is becoming increasingly recognised, and
is not uncommon. It may be as a result of a specific hypogonadal
disorder or age-related decline. It can present in many ways, most
commonly as:
Sexual dysfunction, reduced muscle mass, reduced bone mass with
an increased risk of osteoporosis, reduced facial, body or pubic hair,
small testes, tiredness, depression or non-specific cognitive changes
such as poor concentration.
It may be hypergonadotrophic or hypogonadotrophic:
1. Hypergonadotrophic hypogonadism refers to primary testicular
failure, often with elevated FSH and LH levels. Acquired causes
includes mumps, trauma, torsion, surgery, radiotherapy, drugs
(spironolactone, chemotherapy, marijuana) and myotonic
dystrophy. Congenital disorders include Klinefelters syndrome
(XXY, tall stature, small testes, azoospermia, raised gonadotrophins,
gynaecomastia) and 5a reductase deficiency (androgen resistance).

2. Hypogonadotrophic hypogonadism is gonadic failure secondary
to hypothalamic/pituitary disease, usually with low or normal FSH
and LH levels.
GOITRE/NECK LUMPS
Examine this ladys neck.
This is most likely to be a thyroid case.
Key signs: Swelling in the neck, scar (horizontal skin crease incision is
most common following thyroid surgery), look for regularity/
nodularity/ movement on swallowing, ask the patient to stick her
tongue out (checking for a thyroglossal cyst), work out whether the
thyroid is diffusely enlarged or nodular, look for other evidence of
thyroid problems but most cases but will be well treated in the exam,
look at eyes, some examiners will want you to percuss over the sternum
to check for mediastinal extension.
Table 8.4: Signs in Graves disease and hyperthyroidism
Eye signs
Specific to Graves
Hyperthyroidism
Lid retraction
Lid lag
Proptosis
Chemosis
Exposure keratitis
Ophthalmoplegia
Peripheral signs Thyroid acropachy

Pretibial myxoedema
Agitation
Sweating
Tremor
Palmar erythema
Sinus tachycardia/AF
Brisk reflexes
Check for thyroid status in the hands: Increased sweating

(hyperthyroidism), thyroid acropachy (pseudoclubbing of Graves
disease), pulse (tachycardia or atrial fibrillation in hyperthyroidism,
bradycardia in hypothyroidism), fine tremor (best demonstrated by
placing a sheet of paper on the outstretched hands with the palms
facing downwards). Check also for loss of hair on the upper third on
the eyebrows (hypothyroidism).
Graves disease patients may be hyperthyroid, euthyroid or
hypothyroid depending on their stage of treatment.
Eyes
Features to look for are:
Lid retractionraised upper eyelid but the whiteness of the sclera
is not visible around the iris (Dalyrimples sign).
325
Lid lag.
Proptosis.
Exophthalmosis.
Chemosis (the venous and lymphatic drainage is disturbed by the
protrusion of the eye and the appearance is oedematous and
wrinkled).
Types of goitre include diffuse multinodular, toxic goitre, neoplastic
goitre and autoimmune.
Optic nerve compression: Loss of colour vision initially then develops to
a central scotoma and reduced visual acuity. Papilloedema may occur.
Investigation: Thyroid function tests (TSH and T3/T4), thyroid
antibodies (positive in Hashimotos disease), u/s thyroid (solid versus
cystic), FNAC, bloods (calcium is raised in medullary Ca of the thyroid),
radio-isotope scanning (increased uptake of 131I in Graves, reduced
in thyroiditis). Treatment: -blocker, e.g. propanolol, carbimazole or
propylthiouracid (both thionamides). Block and replace with
thyroxine. Titrate dose and monitor endogenous thyroxine. Stop at
18 months and assess for return of thyrotoxicosis. 1/3 of patients will
remain euthyroid. The dose of carbimazole should be titrated
according to thyroid function tests. The risks of carbimazole are rash
(1:200) and agranulocytosis (1:2000); the patient should attend for a
blood count if they experience a sore throat within the first three
months on medication. If thyrotoxicosis returns, the options are a
repeat course of a thionamide, radioiodine (hypothyroidism common)
and subtotal thyroidectomy.
Severe ophthalmopathy may require high-dose steroids, orbital
irradiation or surgical decompression to prevent visual loss.
Both radioactive iodine therapy and surgical thyroidecomy are
extremely effective and usually result in permanent cure. Patients will
require lifelong thyroxine replacement. Radioiodine is considered to
be the treatment of choice. Treatment with radioiodine may worsen
Graves thyroid eye disease. The exact mechanism by which it does
this may be related to the release of antigens by the damaged thyroid
gland in response to the radioiodine. Currently, it is thought that
radioiodine should not be used in patients with active and/or severe
thyroid eye disease, and in patients with mild eye disease, radioiodine
may be used together with oral corticosteroids (BMJ 1999; 319: 68-9).
Contraindications to radioiodine therapy are breastfeeding and
pregnancy, situations in which it is clear that the safety of other persons
cannot be guaranteed, allergy to iodine, and patients who are

incontinent who are unwilling to have a urinary catheter. Risks include
early hyperthyroidism, late hypothyroidism and late
hyperparathyroidism. Thyroid surgery is expensive and inconvenient,
but offers a definitive cure and leaves a scar. In Graves disease, the
indications for surgery include: A large goitre, the patients preference,
drug non-complance, patients who refuse radiation therapy, patients
wishing to become pregnant within 4 years, and disease relapse when
radioiodine is not available.
Method of Examination
Observe
Is the jugular venous pressure elevated?

Are there any scars?
Are there any enlarged lymph glands visible?
Is there an obvious goitre?
If there is an obvious goitre:

Arrange the patient comfortably in a chair;
Give the patient a glass of water, there is usually one conveniently
nearby. Inspect and palpate the gland from the front;
Stand behind the patient and palpate the gland, one lobe at a time.
The patient should be asked to swallow some water, at appropriate
intervals.
You should be assessing:
Size
Texture
Mobility
Tenderness.
Palpate the cervical lymph glands:
Check for tracheal displacement.
Percuss for retrosternal extension
If there is a thyroidectomy scar, test for Chvosteks sign.
Auscultate over the gland for bruits.
Now perform simple tests of thyroid function:
Observe for myxoedematous facies.
Feel pulse (check rate, rhythm and volume).
Feel palms (sweaty). Look for palmar erythema.
Ask patient to hold hands outstretched. Look for postural tremor.
Inspect for acropachy.
327
Test supinator jerks (observe relaxation phase).

listening over the thyroid for a systolic bruit (this hypervascular
thyroid is almost pathognomic of Graves; disease) (look for other
eye signs above).
Observe shins: Pretibial myxoedema.
Features of Hypothyroidism
Slow pulse, dry skin, cool peripheries, peaches and cream
complexion, periorbital oedema, thinning hair, goitre or thyroidectomy
scar, slow relaxing ankle jerk, pericardial effusion, congestive cardiac
failure, carpal tunnel syndrome (Phalens, Tinels test), proximal
myopathy (stand from sitting) and ataxia. Causes: Autoimmune
(Hashimotos thyroiditis) and atrophic hypothyroidism, iatrogenic
(post thyroidectomy, amiodarone, lithium, antithyroid drugs), iodine
deficiency, dyshormonogenesis. Tests: Thyroid function tests,
autoantibodies, cholesterol, 24-hour urinary collection for cortisol,
pericardial effusion and ischaemia on ECG, pericardial effusion and
CCF on chest X-ray. Management: Thyroxine titrated to TSH
suppression and clinical response.
DYSTHYROID EYE DISEASE

This 42-year-old lady has double vision. What is the underlying
endocrine diagnosis?
Investigations: Thyroid function, ultrasound to see if it is cystic, scan
old spots may be malignant, adenomas are usually hot, FNA if there
are concerns about malignancy.
Management: Check that the airway is secure at least tell the examiner
that this would be a thought, management is then of the underlying
problem thyroxine/radioiodine, etc. as appropriate to case.
PAROTID ENLARGEMENT
This 66-year-old man with a previous alcohol dependence syndrome
has noticed some changes in the appearance in his face. What are the
possibilities here?
Ask the patient whether the parotids are painful and the mouth
dry.
Ask about dry eyes or the use of artificial tears.
Consider history of sarcoidosis, lymphoma or leukaemia.
Examination demonstrates bilateral parotid enlargement.

Causes: Sarcoidosis, Sjogrens syndrome or keratoconjuncivitis sicca,
lymphoma, leukaemia.
Schirmers test: Filter paper is hooked over the lower eyelid.
Manage patients with artificial tears (e.g. hypromellose) and
artificial saliva for dry mouth.
TURNERS SYNDROME
This 42-year-old lady has had fertility problems. What is the
underlying diagnosis?
Turners syndrome (45XO, XO, XX mosaicism) causes primary
amenorrhoea, short stature and delayed puberty. There may be
webbed beck, shield-like chest (broad chest with widely spaced nipples
and poorly developed breasts), short 4th metacarpals, high-arched
palate, numerous naevi, secondary sexual characteristics are underdeveloped, and widely spaced nipples. Sometimes there is a horseshoe
kidney or aortic coarctation. Other features are lymphoedema,
hypertelorism, epicanthal fold, strabismus, ptosis, intestinal
telengectasia, premature osteoporosis, premature ageing in appearance,
higher incidence of diabetes mellitus and Hashimotos thyroiditis.
Examine the cardiological system for coarctation of the aorta and
pulmonary stenosis. Oestrogen levels are low with raised FSH and
LH levels: Turners syndrome (gonadal dysgenesis) is the most
common cause of primary ovarian failure. Congenital renal
abnormalities (horse-shoe kidneys and double ureters) may be present
in some cases. Differential diagnosis for short stature: familial,
achondroplasia (small limbs, relatively normal trunk, large head
bulging), Turners syndrome, Noonans syndrome.
GYNAECOMASTIA
Examine this mans chest (observation only), and discuss with the
examiners.
Make sure that there is gynaecomastia not excessive breast tissue
in an obese person, confirmed on palpation by the presence of
increased glandular tissue. Note for height (Klinefelters syndrome),
acromegalic features, thyrotoxic features, Addisonian features, signs
of cirrhosis, heart failure (spironolactone), atrial fibrillation (digoxin),
clubbing and cachexia (carcinoma of the lung), absence of body hair
(hypogonadism, oestrogen therapy), or an evidence of an endocrine
disorder. Palpate for a testicular tumour.
329
Causes of Gynaecomastia
Physiological: Pubertal (very common, often unilateraldue to transient
dominance of circulating oestradiol over testosterone).
Senile (normal rise in oestrogens and fall in androgens with age).
Pathological
Cirrhosis of the liver.

Thyrotoxicosis.
Carcinoma of the lung and liver.
Klinefelters syndrome (47XXY, small testes, mental deficiency,
incomplete virilization, raised LH and FSH, azoospermia,
cryptochordism, personality disorders, diabetes, chronic
obstructive airways disease: Span > height, sparse body hair, timid
behaviour).
Pituitary disease (acromegaly, hypopituitarism, visual field defect).
Isolated gonadotrophin deficiency (e.g. Kallmans syndrome).
Testicular tumours (due to HCG secretion, oestrogen secretion).
Testicular failure.
Addisons disease.
Adrenal carcinoma.
Testicular femininization.
Drug-induced.
Rare (X-linked androgen-insensitivity; also may cause fasciculations
in the tongue).
Investigations: FBC, ESR, U&Es (renal failure), LFTs (liver failure),

TFTs (thyroid disorders), CXR (primary tumour), mammography,
chromosome analysis (Klinefelters syndrome), HCG and AFP
(testicular tumour), prolactin (prolactinoma), CT head (pituitary
tumour).
PAGETS DISEASE
Simply look at this mans face, arms and legs, and discuss with the
examiners.
There is enlargement of the skull. Bowing of tibia. Warm. Bony
enlargement. Patient may be kyphotic (vertebral involvement may
lead to loss of height and kyphosis from disc degeneration and
verebral collapse). Occurs in 3% of population over 70. Bone pain,
headaches, tinnitus and vertigo. Deafness (conductive) look for
hearing aid. Cardiac failure (high-output), entrapment neuropathies;
optic atrophy and angioid streaks.

Symptoms: Usually asymptomatic, bone pain and tenderness (2%).
Investigations: Grossly elevated serum alkaline phosphatase, urinary
hydroxyproline elevated.
Calcium and phosphate usually normal.
High serum uric acid and high ESR.
Radiology: moth-eaten appearance on plain films (osteoporosis
circumscripta).
Bone scans (increased uptake).
Other complications: Urolithiasis, sarcoma.
Causes of bowing tibia: Pagets disease, rickets, apparent bowing,
congenital syphilis, yaws.
OSTEOMALACIA
This 42-year-old lady who is an Indian lady with coeliac disease has
been under follow-up following initiation of a gluten-free diet. Look
at her legs and discuss what may be the diagnosis.
Legs are bilaterally and symmetrically curved.
Short-stature.
Deformity long-standing.
Diagnosis of old rickets.
Main causes of rickets/osteomalacia:
Decreased availability of vitamin Dinsufficient sunlight exposure,
low dietary intake
Malabsorption: Billroth type II gastrectomy, celiac disease, jejunoileal
bypass, regional enteritis, pancreatic insufficiency, biliary cirrhosis.
Abnormal metabolism: Chronic renal failure, liver disease, X-linked
hypophosphataemia, RTAs, anticonvulsants, vitamin-D resistant rickets
Miscellaneous: Aluminium toxicity, hypophosphataemia, nephritic
syndrome.
EYES
You are likely for this bit to be taken away into a separate darkened
room, if you are asked to examine any eyes.
Look at this patients eyes and discuss the diagnosis with the
examiners.
Examination of fundi
It is helpful to have your own ophthalmoscope with which you are
familiar.
331
Most people find ophthalmoscopy difficult because they become

lost and disorientated within the eye. It you take the time to position
yourself and the patient correctly, you should find it easier to navigate
your way around the fundus.
Introduce yourself.
Observe any external signs, e.g. nystagmus may be present in a
patient with demyelinating eye disease providing a clue to the presence
of optic atrophy.
Instruct the patient to fix his eyes at a point behind you, which is
chosen for height so that you are comfortably able to look into their
eye.
Ask for the room to be darkened to facilitate your examination.
Use your right eye to examine the patients right eye and vice
versa. When examining the right eye, hold the ophthalmoscope in
your right hand and vice versa, placing your index finger on the
rotating disc to allow you to alter the power as necessary.
Before looking at the posterior segment start from 50 cm away,
and look at the red reflex. This provides information about the clarity
of the media in front of the retina, such as the presence of cataracts or
vitreous haemorrhage, which will be of some diagnostic help if the
retina is difficult to visualize.
Move closer to the eye and look at the cornea, anterior chamber,
lens and vitreous in turn. Opacities in any of these media will appear
as black spots against the red reflex.
The optic disc (blind spot) is located 20 degrees of the visual angle
medial/nasal to the macula (centre of fixation). It also lies just below
the horizontal.
Look into the eye from about 20 degrees lateral/temporal to the
line of fixation and from just below the horizontal meridian. The optic
disc should come into view immediately and you need to adjust the
power of the ophthalmoscope to obtain a sharper image. Check for
cupping, colour (pallor/neovascularisation/haemorrhages) and contour
(swelling/drusen).
If the patients eyes have not been dilated for the examination, the
abnormality is usually located at the optic disc.
Next follow each of the four major vascular arcades looking for
abnormalities such as arterio-venous crossings, vessel calibre and
tortuosity.
Examine the peripheral retina in the four quadrants by asking the
patient to look in the direction of each quadrant. Look for the presence
of pigmentary abnormalities, exudates, haemorrhages and new vessels.
Figure 8.2: Diabetic retinopathy

(For colour version, see Plate 1)
Examine the macula by asking the patient to look at the light of

the ophthalmoscope. The macula in health is darker than the
surrounding retina in colour and free of vessels at its centre. It is
located 1 2 disc diameters lateral and a little below the temporal
margin of the optic disc. The central depression, the fovea, should be
identified. Abnormalities in this region will affect visual acuity. Look
for exudates, haemorrhages or drusen.
CATARACT/RUBEOSIS
Causes: Diabetes, old age, trauma, metabolic (Cushings syndrome.
Willsons disease, galactosaemia), congenital disorders such as
dystrophia myotonica, Turners syndrome, congenital infections such
as rubella or cytomegalovirus, dermatological disorders such as atopic
dermatitis/ichthyosis, chronic anterior uveitis, hypoparahyroidism,
radiation, myotonic dystrophy, retinitis pigmentosa, steroid therapy,
chlorpromazine, chloroquine.
DIABETIC RETINOPATHY
This 58-year-old woman has had insulin-dependent diabetes mellitus
(IDDM) for the past 12-years. Examine her fundi to establish whether
or not she has retinopathy and discuss her further management in the
light of your findings (Figure 8.2).
333

Signs
Early background retinopathy (mild non-proliferative diabetic
retinopathy) microaneurysms, sparse scattered haemorrhages, few hard
exudates. Routine 13-week referral time to eye-clinic, annual followup.
Moderate non-proliferative diabetic retinopathy: Hard exudatives.
6 weeks referral. Focal laser treatment. 3 months follow-up.
Maculopathy: Clinically significant macular oedema (CSME), ischaemic
maculopathy (untreatable), CSME, which appears as retinal thickening,
is difficult to appreciate without the aid of binocular vision. Warning
signs include hard exudates (circinate if in the form of rings), which
indicate oedema and multiple haemorrhages indicating the presence of
ischaemia.
Severe non-proliferative: >20 intra-retinal haemorrhages in each of the 4
quadrants, venous beading in 2+ quadrants, intraretinal abnormalities
in 1+ quadrant. 6 weeks referral time and 3 week month follow-up.
Proliferative retinopathy: One or more of the following:
Neovascularization of the retina, optic nerve or iris; vitreous
haemorrhage; pre-retinal haemorrhage + retinal detachment + fibrous
tissue adherent to vitreous face of the retina. 2 weeks referral time
and 2 month follow-up.
Investigations
Ordinary eye examMay not detect non-advanced cases.
Dilated eye exam.
Eye test (vision test)Only detects very advanced cases of
retinopathy
Dye test (fluorescein angiogram)This is a special eye test that
shows retinal circulation.
Amsler gridA special test that helps you identify what parts of
your visual field are damaged.
Slit lamp examinationOften does as part of a dilated eye exam.
This test examines the front or back of the eye.
Colour fundus photography examination (dilated). A form of
photography of the retina.
Eye ultrasound test (ultrasonography). A rarely used test that is
mainly used when there is a vitreous haemorrhage or cataract that
makes a visual dilated eye checkup not possible.

Non-mydiatric camera. A new form of retinal examination for
retinopathy that does not require pupil dilation.
Management
Accelerated deterioration occurs in poor diabetic control, hypertension
and pregnancy.
Control blood sugars (lower blood sugar HBA1c <7.5% is associated
with less retinopathy), quit smoking, control blood pressure (BP < 140/80
improves micro- and macrovascular complication rates), laser eye surgery,
laser photocoagulation, scatter photocoagulation or panretinal
photocoagulation which usually avoids the macular region (prevents the
ischaemic retinal cells secreting angiogenesis factors causing
neovascularization), focal photocoagulation: A focussed attack on certain
retinal areas.
(Indications: Maculopathy, proliferative and pre-proliferative
diabetic retinopathy).
DCCT trial was a 6 year study into the effects of tight glucose
control on microvascular complications in type I diabetes patients.
Patients maintained on intensive insulin regimen showed 54%
reduction in retinopathy.
Table 8.5: Summary table of referral speed for diabetic retinopathy in the UK,
at time of publication
Immediately (1 day)
Urgently (1 week)
Soon (4 weeks)
Sudden loss of vision

Retinal detachment
New vessel formation

Preretinal and/or vitreous
haemorrhage
Rubeosis iridis
Unexplained drop in visual

acuity
Hard exudates within 1 disc
diameter of the fovea
Macular oedema
Unexplained retinal
findings
Pre-proliferative or more
advanced (severe) retinopathy.
PAPILLOEDEMA
Features: Bilateral, disk hyperaemia, indistinct margins, absence of
spontaneous venous pulsation, dilated veins, splinter haemorrhages,
cotton wool spots, hard exudates, optic atrophy (late stage). Causes:
Intra-cranial space-occupying lesion, tumour, abscess, haematoma,
335
benign intracranial hypertension; meningitis; hypercapnoea; sinus

thrombosis. Optic disc swelling causes include ischaemic optic neuropathy, accelerated (malignant) hypertension, pseudopapilloedema;
central retinal vein thrombosis. cavernous hypoparathyroidism;
severe anaemia; Guillain-Barr syndrome, Pagets disease, Hurlers
syndrome, poisoining with vitamin A, tetracyclines, ocular
toxoplasmosis, cereberal anoxia, aqueduct stenosus.
OLD CHOROIDORETINITIS
Scars of old choroidoretinitis appear as well-defined white patches
(where the retina is atrophic) with pigmented edges (due to
proliferation of the retinal pigment epithelium). The blood vessels
can be seen to pass over the lesions undisturbed. Differential diagnosis
of the pigmented retina include normal racial variant, malignant melanoma, retinitis pigmentosa, scans of panretinal photocoagulation.
Causes of choroidoretinitis include cytomegalovirus, congenital
toxoplasmosis, toxocara, AIDS, sarcoidosis, Behcets disease, TB,
syphilis.
DYSTHYROID EYE DISEASE

Key signs: Exopthalmos, look from above in the plane of the forehead;
look for opthalmoplegia; if allowed check for other signs of
hyperthyroidism; visual acuity.
Investigations: Those for thyroid function, visual acuity, MRI of orbit.
Management: If affecting vision, surgical help is critical. Control
hyperthyroidism but this will not necessarily help eyes. Long-term
supervision eye drops/lid surgery/etc. to protect cornea.
OCULAR PALSY AND NYSTAGMUS (SEE NEUROLOGY)

Key signs: III ptosis, large pupil, eye down and out, IV diplopia on
looking down and in, VI horizontal diplopia on looking out.
Investigations: Are for underlying cause, IIIdiabetes, temporal arteritis,
posterior communicating artery aneurysm and tumours which are
more likely to enlarge the pupil and therefore less common in the
exam, IV- trauma history, VI alone Wernickes, false localizing sign
with raised intracranial pressure, pontine stroke (unlikely in the exam).
OPTIC ATROPHY
Figure 8.3: Optic atrophy

Degeneration of the nerve fibre bundles of the optic nerve and their
replacement by glial cells leads to the pale appearance of the optic
disc. Certain characteristics can give a clue as to the cause. In optic
nerve disease (primary optic atrophy), the edges of the disc will be
well defined in contrast to chronic papilloedema where the edge is
indistinct or blurred. In glaucoma, the blood vessels will appear to
dip at the edge of a cupped optic disc. Consider also retinitis
pigmentosa, central retinal artery occlusion, Foster-Kennedy
syndrome (papilloedema in one eye and optic atrophy in the other).
End of bed: Cerebellar signs (Fredreichs ataxia, multiple sclerosis),
large bossed skull (Pagets), Argyll-Robertson pupil.
To confirm findings, look for a central scotoma, abnormalities of
colour perception, and a relative afferent papillary defect.
Key signs: Reduced visual acuity often severe, pale discs, may be signs
of specific problem such as pigmentation with retinitis pigmentosa.
Common Causes
Multiple sclerosis: May be young, ask to examine the central visual
field and the cerebellar system.
Compression of optic nerve by tumour or aneurysm (pituitary or
meningioma).
337
Glaucoma (older patient).

Ischaemic optic atrophy (abrupt onset of visual loss in an elderly
patient); examine the pulse and listen for carotid bruits; giant cell
arteritis or idiopathic acute anterior ION.
Lebers optic atrophy.
Retinal artery occlusion.
Toxic ambylopia (lead, methyl alcohol, arsenic, insecticides,
quinine).
Nutritional amblyopia (tobacco, vitamin B 12 deficiency and
hyperglycaemia in diabetics).
Tabes dorsalis.
Pagets disease.
Trauma (birth hypoxia).
Infections (meningitis, encephalitis, neurosyphilis).
Secondary optic atrophy secondary to chronic papilloedema
Consecutive optic atrophy caused by extensive retinal disease
such as retinitis pigmentosa and chorioretinitis.
Investigations: History including family history, underlying conditions
such as a demyelinating disease or tumours.
Management: Remember practical issues, aids for poor sight,
registration so that patients receive appropriate benefits, is there any
underyling problem to treat, if not support only.
RETINAL VEIN OCCLUSION
Figure 8.4: Retinal vein occlusion


Veins are tortuous and engorged. Haemorrhages are scattered +++
riotously over the whole retina, irregular and superficial, like bundles
of straw along the veins. Multiple cotton wool spots. Optic disc swelling
in the acute stage. Disc collateral vessels, retinal exudates, aterial and
venous sheathing in chronic stages.
Look for diabetic or hypertensive changes.
Rubeosis iridis causes secondary glaucoma (CRVO), visual loss or
field defect.
Risk factors: There may be hypertension, hyperlipidaemia or diabetes
mellitus, or there may be an underlying hyperviscosity syndrome,
especially Waldenstroms macroglobulinaemia, retinal periphlebitis
(sarcoidosis, Behcets disease), collagen vascular disorders. Young
adults: OCP is risk factor. 20% can lose sight in the eye due to acute
secondary glaucoma.
Management: Refer to an ophtlamologist within 2-3 weeks. Principles
of management lie in the prevention of neovascularisation and macular
oedema. Flourescein angiography will define the degree of ischaemia
and hence the risk of neovascularisation. Retinal ischaemia or macular
oedema are treated by panretinal photocoagulation which may
decrease the risk of subsequent neovascular glaucoma.
RETINAL ARTERY OCCLUSION

Features include: Reduced visual acuity, a RAPD, the retinal artery shows
cattle-tracking, cotton wool spots, cherry red spot at the fovea (this is
the intact choroidal circulation which is visible where the retina is at
its thinnest and stands out against the ischaemic milky white macula,
it may disappear after 2 weeks); in chronic cases there is retinal
atrophy, arteriolar swallowing and optic atrophy. Visual field defect,
sectoral retinal ischaemia and changes, embolism may be visible.
Figure 8.5 : Retinal artery occlusion

339
Cherry red spot differential diagnosis: Sphingolipidoses (deposition of

GM2 gangliosidase with the retinal ganglion cells gives the retina a
pale colour), quinine toxicity, traumatic retinal oedema.
Extra points: CauseAF (irregular pulse) or carotid stenosis (bruit).
Effect: Optic atrophy and blind (white stick).
Causes: Emboli from the heart, three types of emboli (cholesterol,
platelet-fibrin emboli associated with large vessel arteriosclerosis and
calcific emboli from cardiac valves), vaso-obliterative disorders,
excessively high intraocular pressure.
This is an ophthalmic emergency. An ophthalmologist must see
the patient within 48 hours of the onset of symptoms.
GLAUCOMA
Figure 8.6: Glaucoma

There is unilateral visual field defect.

This could be due to a space-occupying lesion compressing the
lateral part of the optic chiasma or it could be due to simple glaucoma.
The visual fields are grossly constricted and the patient only has
central vision.
Differential diagnosis: Retinitis pigmentosa, advanced chronic glaucoma
or diffuse choroidoretinitis. In the early stages, a sickle-shaped
extension of the blind spot may be demonstrated and some
impairment of the nasal field may be seen on the Bjerrum screen. The
problem is when to start treatment in a patient with chronic open
angle glaucoma.

In general, patients who have a raised intraocular pressure of 24
mmHg, family history of disease, and those in the 7th decade have
miotics (e.g. pilocarpine) aimed at reducing the intraocular pressure,
hence slowing the progression of visual failure.
There are three cardinal features of POAG:
Raised IOP > 2122 mmHg (> 30 mmHg warrants urgent referral
to an ophthalmologist).
A cupped optic disc with an increased cup: disc ratio.
Visual field loss.
The pathophsiological changes in POAG have been traditionally
been attributed to raised IOP causing damage to the optic nerve head.
Increasingly, however, vascular and toxic damage to the optic nerve
fibres are thought to contribute.
ANGIOID STREAKS
Whilst relatively rare, these are specifically mentioned in the MRCP
Clinical Guidelines.
Dark brown streaks with serrated edges, radiating out from the
optic disc.
Deep to the retinal veins.
Darker and wider than retinal vessels.
Systemic associations are found in 50% of patients. Pseudoxanthoma
elasticum, Pagets disease, Sickle cell anaemia, Ehler-Danlos syndrome,
thrombocytopaenic purpura, Marfans syndrome, acromegaly, lead
poisoning.
MYELINATED OPTIC DISC

A benign congenital abnormality known as medullated or myelinated
nerve fibres. Myelination begins in fetal life at the lateral geniculate
body reaching the optic disc at birth. In 1% of the population
myelination does not stop at the lamina cribrosa but extends onto the
nerve fibres surrounding the optic disc.
Features the optic disc contains a white irregular streaky patch.
The myelination may extend from the disc and terminate peripherally
in a feather-like pattern. It usually obscures the retinal vessels. Look
for other clinical findings associated with myelinated optic disc:
Enlargement of the blind spot, variable visual loss depending on the
extent of myelination, ambylopia (reduced visual acuity in the affected
eye), myopia.
341
HYPERTENSIVE RETINOPATHY
Figure 8.7: Hypertensive retinopathy

Keith-Wagner-Barker classification based on the severity and duration

of hypertension:
Grade I Generalized arteriolar attenuation
Grade II Severe grade I changes, AV nipping, varying vessel calibre
Grade III Haemorrhages, exudates, cotton wool spots
Grade IV Accelerated malignant, optic disc swelling, hypertension
Causes: 90% essential, 10% renal/endocrine/eclampsia/coarctation
of the aorta.
RETINITIS PIGMENTOSA
Figure 8.8: Retinitis pigmentosa


Retinal pigmentary changes in a bone-spicule pattern.
Attenuated retinal vessels.
Pale optic disc.
The pigment conceals the course of retinal vessels. This is in contrast
to choroidoretinitis where the vessels can be traced over the areas of
hyperpigmentation. Also look for associated findings of optic drusen,
optic disc cupping and cataracts. Look for peripheral constriction of
visual fields. You should enquire about a history of night blindness
and take a family history.
RP is a slow degenerative disorder of the rod photoreceptors with
the cones affected late in the disease. Most are registered blind at 40years, with central visual loss in the seventh decade. No treatment.
Patterns of inheritance: Autosomal recessive 51%
Autosomal dominant 26%
X-linked recessive 23%
Secondary RP: Phytanic acid storage disorders (Refsums disease):
Eliminate phtates present in dairy products and green vegetables.
Look for icthyosis.
Kearynes-Sayre disorder. Look for deafness, ophthalmoplegia and
permanent pacemaker.
Abetalipoproteinaemia (Bassen-Kornweig syndrome)
Fredreichs Ataxia
Laurence-Moon-Bardet-Biedle syndrome (polydactyly)
Ushers syndrome
Cockaynes syndrome
Mucopolysaccharidoses (Hurlers syndrome, Hunters syndrome)
Pseudo-RP: Trauma, posterior ocular inflammation, drug toxicity,
following central retinal artery occlusion.
Management: Essential to exclude and treat associated systemic
disease.
Index
A
Abdominal swelling 71
Abnormal liver function tests 72
Acanthosis nigricans 303
Acquiring consent for autopsy
252
Acromegaly 317
Acute
exacerbation 46
stroke 181
Acyanotic heart disease 145
Allergy and facial swelling 105
Alopecia 302
Alzheimers disease 224
Anatomical territory 179
Angioid streaks 340
Ankylosing spondylitis 314
Aortic
incompetence 133
stenosis 130
Apex beat 122
Argyll-Robertson pupils 195
Ascites 14
Aseptic techniques 7
Asthma 52, 64
Atrial septal defect 147
Auscultation technique 124
B
Back pain 82
Beauchamp and Childress
principles 213
Brainstem death and
organ donation 217
Breathlessness/dyspnoea 65
Bronchiectasis 50
Brown-Squard syndrome 188
Bullous disorders 295
Butterfly rash 293
C
Carcinoid syndrome 28
Cardiac failure 62
Cardiovascular system 59
Cataract/rubeosis 332
Cerebellar syndrome 166
Cerebrovascular accident/stroke 177

Cervical myelopathy 190
Charcots joint 310
Chest
pain 60
wall 121
shapes 35
Choice of valve replacement 127
Chronic
liver disease 12
obstructive airways disease 43
Coarctation of aorta 148
Cold and painful fingers 98
Collapse and loss of conciousness 100
Compulsory treatment of TB 268
Confidentiality and good clinical
practice 263
Congenital heart disease 145
Consent for a HIV test 254
Consider particular causes 101
Constrictive pericarditis 120
Cough 67
Court of protection 276
Crohns disease 75
Cushings syndrome 321
Cyanotic heart disease 150
D
Dermatitis herpetiformis 293
Dermatomes 160
Diabetic and peripheral neuropathy 173
Diabetic
foot 316
retinopathy 332
Diagnosed diabetic 231
Diarrhoea 73
Differing patient responses 260
Disorders of
gait 162
higher cortical function 162
Dizziness and funny turns 84
DNAR 273
Doctrine of double effect 269
Double vision 86
Dysphagia 76
Dysthyroid eye disease 327, 335
344
E
Ebsteins anomaly 153
Eczema 289
Ehler-Danlos syndrome 303
Eisenmenger syndrome 150
Emergency
admission to hospital order 251
doctors holding power 250
Empyema 56
Endocarditis prophylaxis 125
Endocrine system 90, 317
Enduring power of attorney 276
Epigastric
mass 33
pain and dyspepsia 77
Epilepsy 265
Erythema nodosum 295
Ethical issues regarding genetic
counselling 258
Euthanasia and assisted suicide 270
Exfoliative dermatitis 304
Extensor plantars and
absent knee jerks 190
Eyes 324, 330
Hormone replacement
therapy (HRT) 235
Horners syndrome 194
Hypercalcaemia 92
Hyperpigmentation 301
Hypertensive retinopathy 341
Hypogonadism 92, 323
Hypopigmentation 302
Hypopituitarism 320
Hypothyroidism 327
I
Inflammatory bowel disease 30
Inhaler technique 39
Inheritance is autosomal dominant 288
Inspection 8, 34, 119
Irregular pulse/atrial fibrillation 125
J
Jaundice 79
Jaw jerk 200
Jehovahs witness 257
Jugular venous pressure 120
Fever of unknown origin 107

Fitness to drive 265
Fredreichs ataxia 185
Kaposis sarcoma 293

Klinefelters syndrome 319
L
G
Gait 307
Galactorrhoea 319
Glaucoma 339
Goitre/neck lumps 324
Gout 315
Gynaecomastia 328, 329
H
Haemochromatosis 26
Haemoptysis 68
Headache 86
Heart sounds 124
Hemiplegia 163
Hepatomegaly 28, 29
Hepatosplenomegaly 33
Hodgkins disease 226
Leg
oedema 296
ulcers 300
Lichen planus 306
Lifestyle adjustments 244
Limbs 154
Lipids 298
Livedo reticularis 306
Locomotor screening GALS 306
Loin pain and haematuria 109
Loss of weight 109
Lower
GI haemorrhage and melaena 80
limbs 159
Lung
cancer 222
collapse 53
malignancy 40
Index
345
Macrocytic anaemia 111

Management of ITP 117
Marfans syndrome 135
Measurement of blood pressure 123
Median nerve palsy 176
Medical
ethics 213
mistake and angry patient 261
Medicolegal aspects of care
of elderly 275
Mental
capacity Act [2005] 251
health Act 250
Metallic prosthetic valve
replacement 126
Microcytic anaemia 110
Mitral
incompetence 139
stenosis 136
valve prolapse 143
Mixed
aortic and mitral valve disease 142
aortic valve disease 135
mitral valve disease 140
Monoarthritis 310
Motor neuron disease 182
Movement disorders 171
MRC classification of power 158
Multiple sclerosis 172, 220
Murmur/endocarditis 63
Muscular dystrophies 188
Myaesthenia gravis 191
Myelinated optic disc 340
Myotonic dystrophy
(dystrophia myotonica) 186
Pagets disease 329

Pain 113
Painful shins 114
Palsies and ptosis 197
Papilloedema 334
Parkinsonism/Parkinsons disease 163
Parotid enlargement 327
Patent ductus arteriosus 149
Pericarditis and pericardial effusion 130
Pigmentary changes 301
Pins and needles 88
Pleural effusion 54
Pneumothorax 54
Polycystic
kidneys/renal enlargement 21
ovarian syndrome 322
Polymyositis and dermatomyositis 305
Polyuria 93
Poor LV function 144
Power of attorney 276
Pretibial myxoedema 299
Primary biliary cirrhosis 32
Proximal myopathy 162
Pruritus 114
Pseudoxanthoma elasticum 303
Psoriasis 290
Psoriatic arthropathy 311
Pulmonary
hypertension 144
stenosis 144
Pulse 121
Pupil reactions 193
Purpura 292
Purpuric rash 116
Pyoderma gangrenosum 296
Necrobiosis lipoidica diabeticorum 297

Needlestick injury 268
Neurofibromatosis 288
Neurological system 82
Radial nerve lesion 177

Reaction and prognosis 216
Recurrence of breast cancer 228
Renal transplant 23, 244
Respiratory function tests 306
Retinal
artery occlusion 338
vein occlusion 337
Retinitis pigmentosa 341
Rheumatoid disease 311
Rheumatological system 98
Road traffic offence 265
O
Ocular palsy and nystagmus 335
Old choroidoretinitis 335
Optic atrophy 336
Osteoarthritis 314
Osteomalacia 330
346
S
Sensory testing 159
Situations where consent is
not possible 248
Skin 287
malignancy 305
Smoking cessation 245
Spastic paraparesis 167
Speech disorders 170
Spine 309
Splenomegaly 17, 18
Statins
239
Steroids 240
Surgical treatments for
medical disorders 242
Syringomyelia 187
Systemic sclerosis 299
T
Testamentary capacity 275
Testicular cancer 225
Tetralogy of Fallot 151
Therapeutic intervention 25
Thyrotoxicosis
233
Tiredness 117
Tone, power, reflexes and
coordination 157
Tonic (Holmes-Adie pupil) 194
Transposition of great arteries 152

Tremor 88
Tricuspid incompetence 142
Tuberculosis 70
Tuberous sclerosis 303
Turners syndrome 328
U
Ulnar nerve palsy 176
Unilateral foot drop 165
Upper limbs 158
V
Ventricular septal defect 145
Visual field testing 196
Vitiligo 290
Vomiting 81
W
Warfarin 237
Wasting of small muscles of hand 192
Weak
legs 89
painful shoulders 98
Weight gain 97
Wheeze 71

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Revision Notes for MRCP 2 PACES

Revision Notes for MRCP 2 PACES

The authors wish to emphasise that whilst there is much factual

The PACES Carousel

What are the Aims of the PACES Examination?

How does the PACES Carousel Work?

Revision Notes for MRCP 2 PACES

stations (stations 2 and 4) to read the introductory material, whilst

Figure 1.1: Carousel of PACES stations

The talking stations, stations 2 and 4, begin with an al limportant

The PACES Carousel 3

Revision Notes for MRCP 2 PACES

The PACES Carousel 5

Revision Notes for MRCP 2 PACES

multiple judgements is primarily in providing feedback to candidates

The PACES Carousel 7

INTRODUCTION TO EXAMINATION TECHNIQUE

METHOD OF EXAMINATION TECHNIQUE

Abdominal System (Station 1)

It is important to observe the general appearance of the patient,

10 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

Left iliac fossa

Carcinoma of the caecum

Carcinoma of the colon

(Causes of an epigastric mass are discussed later)

12 Revision Notes for MRCP 2 PACES

Conclusion of the Examination

CHRONIC LIVER DISEASE

Abdominal System (Station 1)

Spider naevia (small capillary angiomas found in the distribution

14 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

Other measures include serum ascitesAlbumin gradient measurement;

16 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

pressure portal system, and is very effective at stopping bleeding in

18 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

c. Hereditary spherocytosis is a possible cause (icteric, splenomegaly

20 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

tender), sarcoidosis, tuberculosis, brucellosis, toxoplasmosis,

POLYCYSTIC KIDNEYS/RENAL ENLARGEMENT

An Extremely Common Case

22 Revision Notes for MRCP 2 PACES

Abdominal System (Station 1)

renal failure by their 8th decade). Hypertension should be carefully

An Extremely Common Case